Parasympathetic innervation of the heart. Intercellular intracardiac regulatory mechanisms Escape of the heart from the influence of the vagus nerve

Nerves of the heart

The heart receives sensory, sympathetic and parasympathetic innervation. Sympathetic fibers coming from the right and left sympathetic trunks as part of the heart nerves carry impulses that speed up the rhythm of heart contractions and expand the lumen of the coronary arteries, and parasympathetic fibers (an integral part of the cardiac branches of the vagus nerves) conduct impulses that slow down the heart rate and narrow the lumen of the coronary arteries . Sensitive fibers from the receptors of the walls of the heart and its vessels go as part of the cardiac nerves and cardiac branches to the corresponding centers of the spinal cord and brain.

The scheme of innervation of the heart (according to V.P. Vorobyov) can be represented as follows: the sources of innervation of the heart are the cardiac nerves and branches leading to the heart; extraorganic cardiac plexuses (superficial and deep) located near the aortic arch and pulmonary trunk; intraorganic cardiac plexus, which is located in the walls of the heart and is distributed in all their layers.

cardiac nerves(upper, middle and lower cervical, as well as thoracic) start from the cervical and upper thoracic (II-V) nodes of the right and left sympathetic trunks (see "Autonomic nervous system"). The cardiac branches originate from the right and left vagus nerves (see Vagus Nerve).

Superficial extraorganic cardiac plexus lies on the anterior surface of the pulmonary trunk and on the concave semicircle of the aortic arch; deep extraorganic cardiac plexus located behind the aortic arch (in front of the bifurcation of the trachea). The upper left cervical cardiac nerve (from the left upper cervical sympathetic ganglion) and the upper left cardiac branch (from the left vagus nerve) enter the superficial extraorganic cardiac plexus. All other cardiac nerves and cardiac branches mentioned above enter the deep extraorganic cardiac plexus.

Branches of extraorganic cardiac plexuses pass into a single intraorganic cardiac plexus. Depending on which layer of the heart wall it is located in, this single intraorgan cardiac plexus is conventionally divided into closely related subepicardial, intramuscular and subendocardial plexuses. The intraorganic cardiac plexus contains nerve cells and their accumulations, forming small nerve heart nodules, ganglia cardiaca. There are especially many nerve cells in the subepicardial cardiac plexus. According to V.P. Vorobyov, the nerves that make up the subepicardial cardiac plexus have a regular localization (in the form of nodal fields) and innervate certain parts of the heart. Accordingly, six subepicardial cardiac plexuses are distinguished: 1) right front and 2) left front. They are located in the thickness of the anterior and lateral walls of the right and left ventricles on both sides of the arterial cone; 3) anterior atrial plexus- in the anterior wall of the atria; four) right posterior plexus descends from the posterior wall of the right atrium to the posterior wall of the right ventricle (fibers go from it to the sinoatrial node of the conduction system of the heart); 5) left posterior plexus from the lateral wall of the left atrium continues down to the posterior wall of the left ventricle; 6) posterior plexus of the left atrium(plexus of the Gallerian sinus) is located in the upper part of the posterior wall of the left atrium (between the orifices of the pulmonary veins).

Heart - plentiful innervated organ. Among the sensitive formations of the heart, two populations of mechanoreceptors, concentrated mainly in the atria and left ventricle, are of primary importance: A-receptors respond to changes in the tension of the heart wall, and B-receptors are excited when it is passively stretched. Afferent fibers associated with these receptors are part of the vagus nerves. Free sensory nerve endings, located directly under the endocardium, are the terminals of afferent fibers that pass through the sympathetic nerves.

Efferent innervation of the heart carried out with the participation of both departments of the autonomic nervous system. The bodies of sympathetic preganglionic neurons involved in the innervation of the heart are located in the gray matter of the lateral horns of the upper three thoracic segments of the spinal cord. Preganglionic fibers are sent to the neurons of the upper thoracic (stellate) sympathetic ganglion. The postganglionic fibers of these neurons, together with the parasympathetic fibers of the vagus nerve, form the upper, middle, and lower cardiac nerves. Sympathetic fibers permeate the entire organ and innervate not only the myocardium, but also elements of the conduction system.

The bodies of parasympathetic preganglionic neurons involved in innervation of the heart. located in the medulla oblongata. Their axons are part of the vagus nerves. After the vagus nerve enters the chest cavity, branches depart from it, which are included in the composition of the cardiac nerves.

The processes of the vagus nerve, passing through the cardiac nerves, are parasympathetic preganglionic fibers. From them, excitation is transmitted to intramural neurons and then - mainly to the elements of the conduction system. The influences mediated by the right vagus nerve are addressed mainly to the cells of the sinoatrial node, and the left - to the cells of the atrioventricular node. The vagus nerves do not have a direct effect on the ventricles of the heart.

Innervating pacemaker tissue. autonomic nerves are able to change their excitability, thereby causing changes in the frequency of generation of action potentials and heart contractions ( chronotropic effect). Nervous influences change the rate of electrotonic transmission of excitation and, consequently, the duration of the phases of the cardiac cycle. Such effects are called dromotropic.

Since the action of mediators of the autonomic nervous system is to change the level of cyclic nucleotides and energy metabolism, autonomic nerves in general are able to influence the strength of heart contractions ( inotropic effect). Under laboratory conditions, the effect of changing the value of the excitation threshold of cardiomyocytes under the action of neurotransmitters was obtained, it is designated as bathmotropic.

Listed pathways of the nervous system on the contractile activity of the myocardium and the pumping function of the heart are, although extremely important, modulating influences secondary to myogenic mechanisms.

Innervation of the heart and blood vessels

The activity of the heart is regulated by two pairs of nerves: vagus and sympathetic (Fig. 32). The vagus nerves originate in the medulla oblongata, and the sympathetic nerves originate from the cervical sympathetic ganglion. Vagus nerves inhibit cardiac activity. If you start to irritate the vagus nerve with an electric current, then there is a slowdown and even a stop of heart contractions (Fig. 33). After the cessation of irritation of the vagus nerve, the work of the heart is restored.

Rice. 32. Scheme of the innervation of the heart

Rice. 33. Influence of stimulation of the vagus nerve on the heart of a frog

Rice. 34. Influence of stimulation of the sympathetic nerve on the heart of a frog

Under the influence of impulses entering the heart through the sympathetic nerves, the rhythm of cardiac activity increases and each heartbeat intensifies (Fig. 34). This increases the systolic, or shock, blood volume.

If the dog is in a calm state, its heart is reduced from 50 to 90 times in 1 minute. If all the nerve fibers going to the heart are cut, the heart now contracts 120-140 times per minute. If only the vagus nerves of the heart are cut, the heart rate will increase to 200-250 beats per minute. This is due to the influence of the preserved sympathetic nerves. The heart of man and many animals is under the constant restraining influence of the vagus nerves.

The vagus and sympathetic nerves of the heart usually act in concert: if the excitability of the center of the vagus nerve increases, then the excitability of the center of the sympathetic nerve decreases accordingly.

During sleep, in a state of physical rest of the body, the heart slows down its rhythm due to an increase in the influence of the vagus nerve and a slight decrease in the influence of the sympathetic nerve. During physical activity, the heart rate increases. In this case, there is an increase in the influence of the sympathetic nerve and a decrease in the influence of the vagus nerve on the heart. In this way, an economical mode of operation of the heart muscle is ensured.

The change in the lumen of the blood vessels occurs under the influence of impulses transmitted to the walls of the vessels along vasoconstrictor nerves. Impulses from these nerves originate in the medulla oblongata in vasomotor center. The discovery and description of the activities of this center belongs to F.V. Ovsyannikov.

Ovsyannikov Filipp Vasilyevich (1827-1906) - an outstanding Russian physiologist and histologist, full member of the Russian Academy of Sciences, teacher of I.P. Pavlov. FV Ovsyannikov was engaged in the study of the regulation of blood circulation. In 1871, he discovered the vasomotor center in the medulla oblongata. Ovsyannikov studied the mechanisms of respiration regulation, the properties of nerve cells, and contributed to the development of the reflex theory in domestic medicine.

Reflex influences on the activity of the heart and blood vessels

The rhythm and strength of heart contractions change depending on the emotional state of a person, the work he performs. A person's condition also affects the blood vessels, changing their lumen. You often see how, with fear, anger, physical stress, a person either turns pale or, on the contrary, blushes.

The work of the heart and the lumen of the blood vessels are associated with the needs of the body, its organs and tissues in providing them with oxygen and nutrients. The adaptation of the activity of the cardiovascular system to the conditions in which the body is located is carried out by nervous and humoral regulatory mechanisms, which usually function in an interconnected manner. Nervous influences that regulate the activity of the heart and blood vessels are transmitted to them from the central nervous system through the centrifugal nerves. Irritation of any sensitive endings can reflexively cause a decrease or increase in heart contractions. Heat, cold, prick and other stimuli cause excitation at the endings of the centripetal nerves, which is transmitted to the central nervous system and from there it reaches the heart through the vagus or sympathetic nerve.

Experience 15

Immobilize the frog so that it retains its medulla oblongata. Do not destroy the spinal cord! Pin the frog to the board with its belly up. Bare your heart. Count the number of heartbeats in 1 minute. Then use tweezers or scissors to hit the frog on the abdomen. Count the number of heartbeats in 1 minute. The activity of the heart after a blow to the abdomen slows down or even temporarily stops. It happens reflexively. A blow to the abdomen causes excitation in the centripetal nerves, which through the spinal cord reaches the center of the vagus nerves. From here, excitation along the centrifugal fibers of the vagus nerve reaches the heart and slows down or stops its contractions.

Explain why the frog's spinal cord must not be destroyed in this experiment.

Is it possible to cause a frog's heart to stop when it is hit on the abdomen if the medulla oblongata is removed?

The centrifugal nerves of the heart receive impulses not only from the medulla oblongata and spinal cord, but also from the overlying parts of the central nervous system, including from the cerebral cortex. It is known that pain causes an increase in heart rate. If a child was given injections during treatment, then only the appearance of a white coat will cause a conditioned reflex to cause an increase in heart rate. This is also evidenced by the change in cardiac activity in athletes before the start, in pupils and students before exams.

Rice. 35. The structure of the adrenal glands: 1 - the outer, or cortical, layer in which hydrocortisone, corticosterone, aldosterone and other hormones are produced; 2 - the inner layer, or medulla, in which adrenaline and norepinephrine are formed

Impulses from the central nervous system are transmitted simultaneously along the nerves to the heart and from the vasomotor center along other nerves to the blood vessels. Therefore, usually the heart and blood vessels respond reflexively to irritation received from the external or internal environment of the body.

Humoral regulation of blood circulation

The activity of the heart and blood vessels is influenced by chemicals in the blood. So, in the endocrine glands - the adrenal glands - a hormone is produced adrenalin(Fig. 35). It speeds up and enhances the activity of the heart and narrows the lumen of the blood vessels.

At the nerve endings of the parasympathetic nerves, acetylcholine. which dilates the lumen of the blood vessels and slows down and weakens the heart's activity. Some salts also affect the work of the heart. An increase in the concentration of potassium ions slows down the work of the heart, and an increase in the concentration of calcium ions causes an increase in the activity of the heart.

Humoral influences are closely related to the nervous regulation of the activity of the circulatory system. The release of chemicals into the blood and the maintenance of certain concentrations in the blood is regulated by the nervous system.

The activity of the entire circulatory system is aimed at providing the body in different conditions with the necessary amount of oxygen and nutrients, removing metabolic products from cells and organs, and maintaining a constant level of blood pressure. This creates conditions for maintaining the constancy of the internal environment of the body.

Innervation of the heart

The sympathetic innervation of the heart is carried out from centers located in the lateral horns of the three upper thoracic segments of the spinal cord. The preganglionic nerve fibers emanating from these centers go to the cervical sympathetic ganglia and transmit excitation there to neurons, the postganglionic fibers from which innervate all parts of the heart. These fibers transmit their influence to the structures of the heart with the help of the norepinephrine mediator and through p-adrenergic receptors. On the membranes of the contractile myocardium and the conduction system, Pi receptors predominate. There are approximately 4 times more of them than P2 receptors.

The sympathetic centers that regulate the work of the heart, unlike the parasympathetic ones, do not have a pronounced tone. An increase in impulses from the sympathetic nerve centers to the heart occurs periodically. For example, when these centers are activated, caused by reflex, or descending influences from the centers of the trunk, hypothalamus, limbic system and cerebral cortex.

Reflex influences on the work of the heart are carried out from many reflexogenic zones, including from the receptors of the heart itself. In particular, an adequate stimulus for the so-called atrial A-receptors is an increase in myocardial tension and an increase in atrial pressure. The atria and ventricles have B receptors that are activated when the myocardium is stretched. There are also pain receptors that initiate severe pain in case of insufficient oxygen delivery to the myocardium (pain during a heart attack). Impulses from these receptors are transmitted to the nervous system along the fibers passing in the vagus and branches of the sympathetic nerves.

The cardiovascular system provides blood supply to organs and tissues, transporting O 2 , metabolites and hormones to them, delivering CO 2 from tissues to the lungs, and other metabolic products to the kidneys, liver and other organs. This system also carries the cells in the blood. In other words, the main function of the cardiovascular system is transport. This system is also vital for the regulation of homeostasis (for example, to maintain body temperature and acid-base balance).

heart

The circulation of blood through the cardiovascular system is provided by the pumping function of the heart - the continuous work of the myocardium (heart muscle), characterized by alternating systole (contraction) and diastole (relaxation).

From the left side of the heart, blood is pumped into the aorta, through the arteries and arterioles, into the capillaries, where the exchange between blood and tissues takes place. Through the venules, blood is sent to the vein system and then to the right atrium. it systemic circulation- system circulation.

From the right atrium, blood enters the right ventricle, which pumps blood through the vessels of the lungs. it pulmonary circulation- pulmonary circulation.

The heart contracts up to 4 billion times during a person's life, ejecting into the aorta and facilitating the entry of up to 200 million liters of blood into organs and tissues. Under physiological conditions, cardiac output ranges from 3 to 30 l/min. At the same time, the blood flow in various organs (depending on the intensity of their functioning) varies, increasing, if necessary, approximately twice.

shells of the heart

The wall of all four chambers has three shells: endocardium, myocardium and epicardium.

Endocardium lines the inside of the atria, ventricles and valve petals - mitral, tricuspid, aortic valve and pulmonary valve.

Myocardium consists of working (contractile), conductive and secretory cardiomyocytes.

❖ Working cardiomyocytes contain a contractile apparatus and a depot of Ca 2 + (cistern and tubules of the sarcoplasmic reticulum). These cells, with the help of intercellular contacts (intercalary discs), are combined into the so-called cardiac muscle fibers - functional syncytium(the totality of cardiomyocytes within each chamber of the heart).

❖ Conducting cardiomyocytes form the conduction system of the heart, including the so-called pacemakers.

❖ secretory cardiomyocytes. Part of the atrial cardiomyocytes (especially the right one) synthesizes and secretes the vasodilator atriopeptin, a hormone that regulates blood pressure.

Myocardial functions: excitability, automatism, conduction and contractility.

Under the influence of various influences (nervous system, hormones, various drugs), myocardial functions change: the effect on heart rate (i.e., automatism) is denoted by the term "chronotropic action"(can be positive and negative), on the strength of contractions (i.e. on contractility) - "inotropic action"(positive or negative), on the speed of atrioventricular conduction (which reflects the conduction function) - "dromotropic action"(positive or negative), excitability - "batmotropic action"(also positive or negative).

epicardium forms the outer surface of the heart and passes (practically merged with it) into the parietal pericardium - the parietal sheet of the pericardial sac containing 5-20 ml of pericardial fluid.

Heart valves

The effective pumping function of the heart depends on the unidirectional movement of blood from the veins to the atria and further to the ventricles, created by four valves (at the entrance and exit of both ventricles, Fig. 23-1). All valves (atrioventricular and semilunar) close and open passively.

Atrioventricular valves- tricuspid valve in the right ventricle and bivalve(mitral) valve in the left - prevent the reverse flow of blood from the ventricular

Rice. 23-1. Heart valves.Left- transverse (in the horizontal plane) sections through the heart, mirrored with respect to the diagrams on the right. On right- frontal sections through the heart. Up- diastole, at the bottom- systole

Cove in the atria. The valves close when the pressure gradient is directed towards the atria - i.e. when ventricular pressure exceeds atrial pressure. When the pressure in the atria rises above the pressure in the ventricles, the valves open. Semilunar valves - aortic valve and pulmonary valve- located at the exit from the left and right ventricular

kov, respectively. They prevent the return of blood from the arterial system to the cavity of the ventricles. Both valves are represented by three dense, but very flexible "pockets", having a crescent shape and attached symmetrically around the valve ring. The “pockets” open into the lumen of the aorta or pulmonary trunk, so when the pressure in these large vessels begins to exceed the pressure in the ventricles (i.e., when the latter begin to relax at the end of systole), the “pockets” straighten out with blood filling them under pressure, and tightly close along their free edges - the valve slams (closes).

Heart sounds

Listening (auscultation) with a stethophonendoscope of the left half of the chest allows you to hear two heart sounds: I tone and II heart sound. I tone is associated with the closure of the atrioventricular valves at the beginning of systole, II - with the closure of the semilunar valves of the aorta and pulmonary artery at the end of systole. The reason for the occurrence of heart sounds is the vibration of tense valves immediately after closure, together with the vibration of the adjacent vessels, the wall of the heart and large vessels in the region of the heart.

The duration of tone I is 0.14 s, II - 0.11 s. II heart sound has a higher frequency than I. The sound of I and II heart sounds most closely conveys the combination of sounds when pronouncing the phrase "LAB-DAB". In addition to I and II tones, sometimes you can listen to additional heart sounds - III and IV, in the vast majority of cases reflecting the presence of cardiac pathology.

Blood supply to the heart

The wall of the heart is supplied with blood by the right and left coronary (coronary) arteries. Both coronary arteries originate from the base of the aorta (near the insertion of the aortic valve cusps). The posterior wall of the left ventricle, some parts of the septum, and most of the right ventricle are supplied by the right coronary artery. The rest of the heart receives blood from the left coronary artery.

When the left ventricle contracts, the myocardium compresses the coronary arteries, and the blood flow to the myocardium practically stops - 75% of the blood flows through the coronary arteries to the myocardium during relaxation of the heart (diastole) and low resistance of the vascular wall. For adequate coronary

blood flow diastolic blood pressure should not fall below 60 mm Hg.

During exercise, coronary blood flow increases, which is associated with an increase in the work of the heart to supply the muscles with oxygen and nutrients. The coronal veins, collecting blood from most of the myocardium, flow into the coronary sinus in the right atrium. From some areas, located mainly in the "right heart", blood flows directly into the heart chambers.

Innervation of the heart

The work of the heart is controlled by the cardiac centers of the medulla oblongata and the bridge through the parasympathetic and sympathetic fibers (Fig. 23-2). Cholinergic and adrenergic (mainly unmyelinated) fibers form several nerve plexuses in the heart wall containing intracardiac ganglia. Accumulations of ganglia are mainly concentrated in the wall of the right atrium and in the region of the mouths of the vena cava.

parasympathetic innervation. Preganglionic parasympathetic fibers for the heart run in the vagus nerve on both sides. Right vagus nerve fibers innervate

Rice. 23-2. Innervation of the heart. 1 - sinoatrial node; 2 - atrioventricular node (AV node)

right atrium and form a dense plexus in the region of the sinoatrial node. The fibers of the left vagus nerve approach predominantly the AV node. That is why the right vagus nerve affects mainly the heart rate, and the left one - on AV conduction. The ventricles have less pronounced parasympathetic innervation. Effects of parasympathetic stimulation: the force of atrial contractions decreases - a negative inotropic effect, the heart rate decreases - a negative chronotropic effect, the atrioventricular conduction delay increases - a negative dromotropic effect.

sympathetic innervation. Preganglionic sympathetic fibers for the heart come from the lateral horns of the upper thoracic segments of the spinal cord. Postganglionic adrenergic fibers are formed by axons of neurons in the ganglia of the sympathetic nerve chain (stellate and partly superior cervical sympathetic ganglions). They approach the organ as part of several cardiac nerves and are evenly distributed throughout all parts of the heart. The terminal branches penetrate the myocardium, accompany the coronary vessels and approach the elements of the conduction system. The atrial myocardium has a higher density of adrenergic fibers. Every fifth cardiomyocyte of the ventricles is supplied with an adrenergic terminal, ending at a distance of 50 μm from the plasmolemma of the cardiomyocyte. Effects of sympathetic stimulation: the force of atrial and ventricular contractions increases - a positive inotropic effect, heart rate increases - a positive chronotropic effect, the interval between contractions of the atria and ventricles (i.e. conduction delay in the AV connection) is shortened - a positive dromotropic effect.

afferent innervation. Sensory neurons of the ganglia of the vagus nerves and spinal nodes (C 8 -Th 6) form free and encapsulated nerve endings in the wall of the heart. Afferent fibers run as part of the vagus and sympathetic nerves.

PROPERTIES OF THE MYOCARDIA

The main properties of the heart muscle are excitability, automatism, conductivity, contractility.

Excitability

Excitability - the property to respond to irritation with electrical excitation in the form of changes in membrane potential (MP)

followed by PD generation. Electrogenesis in the form of MPs and APs is determined by the difference in ion concentrations on both sides of the membrane, as well as by the activity of ion channels and ion pumps. Through the pore of the ion channels, ions flow along an electrochemical gradient, while ion pumps ensure the movement of ions against the electrochemical gradient. In cardiomyocytes, the most common channels are for Na +, K +, Ca 2 + and Cl - ions.

The resting MP of the cardiomyocyte is -90 mV. Stimulation generates a propagating AP that causes contraction (Fig. 23-3). Depolarization develops rapidly, as in skeletal muscle and nerve, but, unlike the latter, MP does not return to its original level immediately, but gradually.

Depolarization lasts about 2 ms, the plateau phase and repolarization last 200 ms or more. As in other excitable tissues, changes in the extracellular K+ content affect MP; changes in the extracellular concentration of Na + affect the value of AP.

❖ Rapid initial depolarization (phase 0) arises due to the opening of voltage-dependent fast Na + channels, Na + ions quickly rush into the cell and change the charge of the inner surface of the membrane from negative to positive.

❖ Initial fast repolarization (phase 1)- the result of the closing of Na + channels, the entry of Cl - ions into the cell and the exit of K + ions from it.

❖ Subsequent long plateau phase (phase 2- MP remains approximately at the same level for some time) - the result of the slow opening of voltage-dependent Ca 2 + channels: Ca 2 + ions enter the cell, as well as Na + ions, while the current of K + ions from the cell is maintained.

❖ Ultimate rapid repolarization (phase 3) occurs as a result of the closure of Ca 2 + channels against the background of the continued release of K + from the cell through K + channels.

❖ In the resting phase (phase 4) MF is restored due to the exchange of Na + ions for K + ions through the functioning of a specialized transmembrane system - Na + -K + -pump. These processes relate specifically to the working cardiomyocyte; in pacemaker cells, phase 4 is somewhat different.

Automatism and Conductivity

Automatism - the ability of pacemaker cells to initiate excitation spontaneously, without the participation of neurohumoral control. Stimulation that causes the heart to contract occurs in

Rice. 23-3. ACTION POTENTIALS. BUT- ventricle. B- sinoatrial node. AT- ionic conductivity. I - PD recorded from surface electrodes; II - intracellular registration of AP; III - Mechanical response. G- myocardial contraction. ARF - absolute refractory phase; RRF - relative refractory phase. 0 - depolarization; 1 - initial fast repolarization; 2 - plateau phase; 3 - final fast repolarization; 4 - initial level

Rice. 23-3.The ending

specialized conducting system of the heart and spreads through it to all parts of the myocardium.

conduction system of the heart. The structures that make up the conduction system of the heart are the sinoatrial node, the internodal atrial pathways, the AV junction (the lower part of the atrial conduction system adjacent to the AV node, the AV node itself, the upper part of the His bundle), the His bundle and its branches, Purkinje fiber system (Fig. 23-4).

Pacemakers. All departments of the conducting system are capable of generating AP with a certain frequency, which ultimately determines the heart rate, i.e. be the pacemaker. However, the sinoatrial node generates AP faster than other parts of the conduction system, and depolarization from it spreads to other parts of the conduction system before they begin to spontaneously excite. In this way, sinoatrial node - the leading pacemaker, or a first-order pacemaker. The frequency of its spontaneous discharges determines the heart rate (average 60-90 per minute).

Pacemaker potentials

MP of pacemaker cells after each AP returns to the threshold level of excitation. This potential, called

Time (seconds)

Rice. 23-4. CONDUCTION SYSTEM OF THE HEART AND ITS ELECTRIC POTENTIALS.Left- conducting system of the heart.On right- typical PD[sinus (sinoatrial) and AV nodes (atrioventricular), other parts of the conduction system and atrial and ventricular myocardium] in correlation with the ECG.

Rice. 23-5. DISTRIBUTION OF EXCITATION THROUGH THE HEART. A. Potentials of the pacemaker cell. IK, 1Са d, 1Са в - ion currents corresponding to each part of the pacemaker potential. B-E. Distribution of electrical activity in the heart. 1 - sinoatrial node; 2 - atrioventricular (AV) node

prepotential (pacemaker potential) - trigger for the next potential (Fig. 23-6A). At the peak of each AP after depolarization, a potassium current appears, leading to the launch of repolarization processes. When the potassium current and the output of K+ ions decrease, the membrane begins to depolarize, forming the first part of the prepotential. Ca 2 + channels of two types open: temporarily opening Ca 2 + v channels and long-acting Ca 2 + d channels. The calcium current flowing through the Ca 2 + in -channels forms a prepotential, the calcium current in the Ca 2 + d -channels creates AP.

Spread of excitation through the heart muscle

The depolarization that occurs in the sinoatrial node spreads radially through the atria and then converges (converges) at the AV junction (Figure 23-5). Atrial depolarization

the action is completely completed within 0.1 s. Since conduction in the AV node is slower than conduction in the atrial and ventricular myocardium, an atrioventricular (AV-) delay of 0.1 s occurs, after which excitation spreads to the ventricular myocardium. The duration of the atrioventricular delay decreases with stimulation of the sympathetic nerves of the heart, while under the influence of stimulation of the vagus nerve, its duration increases.

From the base of the interventricular septum, the depolarization wave propagates at high speed through the system of Purkinje fibers to all parts of the ventricle within 0.08-0.1 s. Depolarization of the ventricular myocardium begins on the left side of the interventricular septum and spreads primarily to the right through the middle part of the septum. The wave of depolarization then travels down the septum to the apex of the heart. Along the wall of the ventricle, it returns to the AV node, passing from the subendocardial surface of the myocardium to the subepicardial.

Contractility

The property of myocardial contractility is provided by the contractile apparatus of cardiomyocytes connected into a functional syncytium with the help of ion-permeable gap junctions. This circumstance synchronizes the spread of excitation from cell to cell and the contraction of cardiomyocytes. An increase in the force of contraction of the ventricular myocardium - a positive inotropic effect of catecholamines - is mediated by β 1 -adrenergic receptors (sympathetic innervation also acts through these receptors) and cAMP. Cardiac glycosides also increase the contraction of the heart muscle, exerting an inhibitory effect on Na +, K + -ATPase in the cell membranes of cardiomyocytes.

ELECTROCARDIOGRAPHY

Myocardial contractions are accompanied (and caused) by high electrical activity of cardiomyocytes, which forms a changing electric field. Fluctuations in the total potential of the electric field of the heart, representing the algebraic sum of all AP (see Fig. 23-4), can be registered from the surface of the body. Registration of these fluctuations in the potential of the electric field of the heart during the cardiac cycle is carried out when recording an electrocardiogram (ECG) - a sequence of positive and negative teeth (periods of electrical activity of the myocardium), some of which connect

the so-called isoelectric line (the period of electrical rest of the myocardium).

Electric field vector(Fig. 23-6A). In each cardiomyocyte, during its depolarization and repolarization, positive and negative charges closely adjacent to each other (elementary dipoles) appear at the border of the excited and unexcited areas. In the heart, many dipoles simultaneously arise, the direction of which is different. Their electromotive force is a vector characterized not only by magnitude, but also by direction (always from a smaller charge (-) to a larger one (+)). The sum of all vectors of elementary dipoles forms a total dipole - the vector of the electric field of the heart, constantly changing in time depending on the phase of the cardiac cycle. Conventionally, it is believed that in any phase the vector comes from one point, called the electrical center. A significant part of the re-

Rice. 23-6. ELECTRIC FIELD VECTORS OF THE HEART. A. Scheme for constructing an ECG using vector electrocardiography. The three main resultant vectors (atrial depolarization, ventricular depolarization, and ventricular repolarization) form three loops in vector electrocardiography; when these vectors are scanned along the time axis, a normal ECG curve is obtained. B. Einthoven's triangle. Explanation in the text. α - the angle between the electrical axis of the heart and the horizontal

The resulting vectors are directed from the base of the heart to its apex. There are three main resultant vectors: atrial depolarization, ventricular depolarization and repolarization. Direction of the resulting ventricular depolarization vector - electrical axis of the heart(EOS).

Einthoven triangle. In a bulk conductor (human body), the sum of the electric field potentials at three vertices of an equilateral triangle with an electric field source in the center of the triangle will always be zero. Nevertheless, the potential difference of the electric field between the two vertices of the triangle will not be equal to zero. Such a triangle with a heart in its center - Einthoven's triangle - is oriented in the frontal plane of the body (Fig. 23-6B); when taking an ECG, a triangle is artificially created by placing electrodes on both arms and left leg. Two points of the Einthoven triangle with a potential difference between them that changes over time are denoted as derivation of the ECG.

ECG leads. The points for the formation of leads (there are only 12 of them when recording a standard ECG) are the vertices of the Einthoven triangle (standard leads), triangle center (reinforced leads) and points located on the anterior and lateral surfaces of the chest above the heart (chest leads).

Standard leads. The vertices of Einthoven's triangle are the electrodes on both arms and left leg. When determining the potential difference in the electric field of the heart between the two vertices of the triangle, they speak of ECG recording in standard leads (Fig. 23-8A): between the right and left hands - I standard lead, the right hand and left foot - II standard lead, between the left hand and left leg - III standard lead.

Strengthened limb leads. In the center of Einthoven's triangle, when the potentials of all three electrodes are summed up, a virtual "zero", or indifferent, electrode is formed. The difference between the zero electrode and the electrodes at the vertices of Einthoven's triangle is recorded when taking an ECG in enhanced limb leads (Fig. 23-7B): aVL - between the "zero" electrode and the electrode on the left hand, and VR - between the "zero" electrode and the electrode on right hand, aVF - between the "zero" electrode and the electrode on the left leg. The leads are called reinforced because they have to be amplified due to the small (compared to standard leads) electric field potential difference between the top of Einthoven's triangle and the "zero" point.

Rice. 23-7. ECG LEADS. A. Standard leads. B. Strengthened limb leads. B. Chest leads. D. Variants of the position of the electrical axis of the heart depending on the value of the angle α. Explanations in the text

chest leads- points on the body surface located directly above the heart on the anterior and lateral surfaces of the chest (Fig. 23-7B). The electrodes installed at these points are called chest, as well as leads (formed when determining the potential difference in the electric field of the heart between the point of establishment of the chest electrode and the "zero" electrode) - chest leads V 1, V 2, V 3, V 4, V 5, V6.

Electrocardiogram

A normal electrocardiogram (Fig. 23-8B) consists of the main line (isoline) and deviations from it, called teeth-

Rice. 23-8. TEETH AND INTERVALS. A. Formation of ECG teeth during sequential excitation of the myocardium. B, Waves of the normal PQRST complex. Explanations in the text

mi and denoted by the Latin letters P, Q, R, S, T, U. ECG segments between adjacent teeth are segments. The distances between different teeth are intervals.

The main teeth, intervals and segments of the ECG are shown in fig. 23-8B.

P wave corresponds to the coverage of excitation (depolarization) of the atria. The duration of the P wave is equal to the time of passage of excitation from the sinoatrial node to the AV junction and normally does not exceed 0.1 s in adults. Amplitude P - 0.5-2.5 mm, maximum in lead II.

Interval PQ(R) determined from the beginning of the P wave to the beginning of the Q wave (or R if Q is absent). The interval is equal to the transit time

excitation from the sinoatrial node to the ventricles. Normally, in adults, the duration of the PQ (R) interval is 0.12-0.20 s with a normal heart rate. With tachyor bradycardia, PQ(R) changes, its normal values ​​are determined according to special tables.

QRS complex equal to the depolarization time of the ventricles. It consists of Q, R and S waves. The Q wave is the first downward deviation from the isoline, the R wave is the first deviation from the upward isoline after the Q wave. The S wave is a downward deviation from the isoline following the R wave. The QRS interval is measured from the beginning of the Q wave (or R, if Q is absent) to the end of the S wave. Normally, in adults, the QRS duration does not exceed 0.1 s.

ST segment- the distance between the end point of the QRS complex and the beginning of the T wave. Equal to the time during which the ventricles remain in a state of excitation. For clinical purposes, the position of the ST relative to the isoline is important.

T wave corresponds to ventricular repolarization. T anomalies are nonspecific. They can occur in healthy individuals (asthenics, athletes), with hyperventilation, anxiety, drinking cold water, fever, rising to a high altitude above sea level, as well as with organic myocardial damage.

U wave- a slight upward deviation from the isoline, recorded in some people after the T wave, most pronounced in leads V 2 and V 3. The nature of the tooth is not exactly known. Normally, its maximum amplitude is not more than 2 mm or up to 25% of the amplitude of the previous T wave.

QT interval represents the electrical systole of the ventricles. It is equal to the time of ventricular depolarization, varies depending on age, sex and heart rate. It is measured from the beginning of the QRS complex to the end of the T wave. Normally, in adults, the duration of QT ranges from 0.35 to 0.44 s, but its duration is very dependent on heart rate.

Normal heart rhythm. Each contraction originates in the sinoatrial node (sinus rhythm). At rest, the heart rate fluctuates between 60-90 per minute. Heart rate decreases (bradycardia) during sleep and increases (tachycardia) under the influence of emotions, physical work, fever and many other factors. At a young age, the heart rate increases during inhalation and decreases during exhalation, especially with deep breathing, - sinus respiratory arrhythmia(standard version). Sinus respiratory arrhythmia is a phenomenon that occurs due to fluctuations in the tone of the vagus nerve. During inhalation,

pulses from lung stretch receptors inhibit the inhibitory effects on the heart of the vasomotor center in the medulla oblongata. The number of tonic discharges of the vagus nerve, which constantly restrain the rhythm of the heart, decreases, and the heart rate increases.

Electrical axis of the heart

The greatest electrical activity of the myocardium of the ventricles is found during their excitation. In this case, the resultant of the emerging electrical forces (vector) occupies a certain position in the frontal plane of the body, forming an angle α (it is expressed in degrees) relative to the horizontal zero line (I standard lead). The position of this so-called electrical axis of the heart (EOS) is estimated by the size of the teeth of the QRS complex in standard leads (Fig. 23-7D), which allows you to determine the angle α and, accordingly, the position of the electrical axis of the heart. The angle α is considered positive if it is located below the horizontal line, and negative if it is located above. This angle can be determined by geometric construction in Einthoven's triangle, knowing the size of the teeth of the QRS complex in two standard leads. In practice, special tables are used to determine the angle α (the algebraic sum of the teeth of the QRS complex in I and II standard leads is determined, and then the angle α is found from the table). There are five options for the location of the axis of the heart: normal, vertical position (intermediate between the normal position and rightogram), deviation to the right (rightogram), horizontal (intermediate between the normal position and leftogram), deviation to the left (leftogram).

Approximate assessment of the position of the electrical axis of the heart. To memorize the differences between a right-gram and a left-gram, students use a witty school trick, which consists in the following. When examining their palms, the thumb and forefinger are bent, and the remaining middle, ring and little fingers are identified with the height of the R wave. They “read” from left to right, like a regular line. The left hand is a levogram: the R wave is maximum in standard lead I (the first highest finger is the middle one), decreases in lead II (ring finger), and is minimal in lead III (little finger). The right hand is a rightogram, where the situation is reversed: the R wave grows from lead I to lead III (as well as the height of the fingers: little finger, ring finger, middle finger).

Causes of deviation of the electrical axis of the heart. The position of the electrical axis of the heart depends on both cardiac and non-cardiac factors.

In people with a high standing diaphragm and / or a hypersthenic constitution, the EOS takes a horizontal position or even a levogram appears.

In tall, thin people with a low diaphragm, the EOS is normally located more vertically, sometimes up to a rightogram.

PUMPING FUNCTION OF THE HEART

Cardiac cycle

The cardiac cycle lasts from the beginning of one contraction to the beginning of the next and begins in the sinoatrial node with the generation of AP. An electrical impulse leads to excitation of the myocardium and its contraction: the excitation sequentially covers both atria and causes atrial systole. Further, excitation through the AV connection (after AV delay) spreads to the ventricles, causing the systole of the latter, an increase in pressure in them and the expulsion of blood into the aorta and pulmonary artery. After the ejection of blood, the ventricular myocardium relaxes, the pressure in their cavities drops, and the heart prepares for the next contraction. Sequential phases of the cardiac cycle are shown in Fig. 23-9, and sum-

Rice. 23-9. Cardiac cycle. Scheme. A - atrial systole. B - isovolemic contraction. C - fast exile. D - slow ejection. E - isovolemic relaxation. F - fast filling. G - slow filling

Rice. 23-10. Summary characteristic of the heart cycle. A - atrial systole. B - isovolemic contraction. C - fast exile. D - slow ejection. E - isovolemic relaxation. F - fast filling. G - slow filling

Marginal characteristic of various events of the cycle in fig. 23-10 (the phases of the cardiac cycle are indicated by Latin letters from A to G).

Atrial systole(A, duration 0.1 s). The pacemaker cells of the sinus node depolarize, and excitation spreads through the atrial myocardium. A P wave is recorded on the ECG (see Fig. 23-10, lower part of the figure). Atrial contraction increases pressure and causes additional (in addition to gravity) flow of blood into the ventricle, slightly increasing the end-diastolic pressure in the ventricle. The mitral valve is open, the aortic valve is closed. Normally, 75% of the blood from the veins flows through the atria directly into the ventricles by gravity, before the atrial contraction. Atrial contraction adds 25% of the blood volume as the ventricles fill.

Ventricular systole(B-D, duration 0.33 s). The excitation wave passes through the AV junction, His bundle, Purky fibers

nee and reaches myocardial cells. Ventricular depolarization is expressed by the QRS complex on the ECG. The onset of ventricular contraction is accompanied by an increase in intraventricular pressure, closure of the atrioventricular valves, and the appearance of a first heart sound.

Period of isovolemic (isometric) contraction (B). Immediately after the start of contraction of the ventricle, the pressure in it rises sharply, but changes in intraventricular volume do not occur, since all valves are tightly closed, and blood, like any liquid, is not compressible. It takes from 0.02 to 0.03 s for the ventricle to develop pressure on the semilunar valves of the aorta and pulmonary artery, sufficient to overcome their resistance and open. Therefore, during this period, the ventricles contract, but the expulsion of blood does not occur. The term "isovolemic (isometric) period" means that there is tension in the muscle, but there is no shortening of the muscle fibers. This period coincides with the minimum systemic pressure, called diastolic blood pressure for the systemic circulation.

Period of exile (C, D). As soon as the pressure in the left ventricle becomes higher than 80 mm Hg. (for the right ventricle - above 8 mm Hg), the semilunar valves open. Blood immediately begins to leave the ventricles: 70% of the blood is ejected from the ventricles in the first third of the ejection period and the remaining 30% in the next two thirds. Therefore, the first third is called the period of rapid exile. (C) and the remaining two-thirds - a period of slow exile (D). Systolic blood pressure (maximum pressure) serves as the dividing point between the period of fast and slow ejection. Peak BP follows peak blood flow from the heart.

end of systole coincides with the occurrence of the second heart sound. The force of muscle contraction decreases very quickly. There is a reverse flow of blood in the direction of the semilunar valves, closing them. The rapid drop in pressure in the cavity of the ventricles and the closure of the valves contribute to the vibration of their strained valves, creating a second heart sound.

Ventricular diastole(E-G) has a duration of 0.47 s. During this period, an isoelectric line is recorded on the ECG until the beginning of the next PQRST complex.

Period of isovolemic (isometric) relaxation (E). AT

during this period, all valves are closed, the volume of the ventricles is unchanged. The pressure drops almost as fast as it increased during

isovolemic contraction time. As blood continues to flow into the atria from the venous system, and ventricular pressure approaches the diastolic level, atrial pressure reaches its maximum.

Filling period (F, G). Rapid filling period (F)- the time during which the ventricles quickly fill with blood. The pressure in the ventricles is less than in the atria, the atrioventricular valves are open, blood from the atria enters the ventricles, and the volume of the ventricles begins to increase. As the ventricles fill, the compliance of the myocardium of their walls decreases, and the filling rate decreases (the period of slow filling, G).

Volumes

During diastole, the volume of each ventricle increases to an average of 110-120 ml. This volume is known as end-diastolic volume. After ventricular systole, the blood volume decreases by about 70 ml - the so-called stroke volume of the heart. Remaining after completion of ventricular systole end systolic volume is 40-50 ml.

If the heart contracts more than usual, then the end-systolic volume decreases by 10-20 ml. If a large amount of blood enters the heart during diastole, the end-diastolic volume of the ventricles may increase up to 150-180 ml. The combined increase in end-diastolic volume and decrease in end-systolic volume can double the stroke volume of the heart compared to normal.

Diastolic and systolic blood pressure

The mechanics of the left ventricle is determined by diastolic and systolic pressure in its cavity.

diastolic pressure in the cavity of the left ventricle is created by a progressively increasing amount of blood; The pressure just before systole is called end-diastolic. Until the volume of blood in the noncontracting ventricle exceeds 120 ml, the diastolic pressure remains practically unchanged, and at this volume the blood freely enters the ventricle from the atrium. After 120 ml, diastolic pressure in the ventricle rises rapidly, partly because the fibrous tissue of the wall of the heart and pericardium (and partly also the myocardium) have exhausted the possibilities of their extensibility.

Systolic pressure in the left ventricle. During ventricular contraction, systolic pressure increases even in

conditions of a small volume, but reaches a maximum with a ventricular volume of 150-170 ml. If the volume increases even more, then the systolic pressure drops, because the actin and myosin filaments of the muscle fibers of the myocardium are stretched too much. The maximum systolic pressure for a normal left ventricle is 250-300 mm Hg, but it varies depending on the strength of the heart muscle and the degree of stimulation of the cardiac nerves. In the right ventricle, the maximum systolic pressure is normally 60-80 mm Hg.

Under normal conditions, an increase in preload causes an increase in cardiac output according to the Frank-Starling law (the force of contraction of a cardiomyocyte is proportional to the amount of its stretch). An increase in afterload initially reduces stroke volume and cardiac output, but then the blood remaining in the ventricles after weakened heart contractions accumulates, stretches the myocardium and, also according to the Frank-Starling law, increases stroke volume and cardiac output.

Work done by the heart

Stroke volume- the amount of blood expelled by the heart with each contraction. Striking performance of the heart- the amount of energy of each contraction, converted by the heart into work to promote blood in the arteries. The value of impact performance (SP) is calculated by multiplying the stroke volume (SV) by blood pressure.

UP = UO xAD

The higher the BP or SV, the greater the work done by the heart. Impact performance also depends on preload. Increasing preload (end-diastolic volume) improves impact performance.

Cardiac output(SV; minute volume) is equal to the product of stroke volume and the frequency of contractions (HR) per minute.

SV = UO χ heart rate

Minute performance of the heart(MPS) is the total amount of energy converted into work in one minute. It is equal to percussion performance multiplied by the number of contractions per minute.

MPS = AP χ HR

Control of the pumping function of the heart

At rest, the heart pumps from 4 to 6 liters of blood per minute, per day - up to 8-10 thousand liters of blood. Hard work is accompanied by a 4-7-fold increase in the pumped blood volume. The basis for the control of the pumping function of the heart is: 1) its own cardiac regulatory mechanism, which reacts in response to changes in the volume of blood flowing to the heart (Frank-Starling law), and 2) control of the frequency and strength of the heart by the autonomic nervous system.

Heterometric self-regulation (Frank-Starling mechanism)

The amount of blood pumped by the heart every minute depends almost entirely on the flow of blood into the heart from the veins, denoted by the term "venous return". The inherent ability of the heart to adapt to changes in the volume of incoming blood is called the Frank-Starling mechanism (law): the more the heart muscle is stretched by the incoming blood, the greater the force of contraction and the more blood enters the arterial system. Thus, the presence of a self-regulatory mechanism in the heart, determined by changes in the length of myocardial muscle fibers, allows us to speak of heterometric self-regulation of the heart.

In the experiment, the effect of changes in the magnitude of venous return on the pumping function of the ventricles is demonstrated on the so-called cardiopulmonary preparation (Fig. 23-11A).

The molecular mechanism of the Frank-Starling effect is that the stretching of myocardial fibers creates optimal conditions for the interaction of myosin and actin filaments, which allows generating contractions of greater force.

Factors regulating end-diastolic volume under physiological conditions

❖ Stretching of cardiomyocytes increases under the influence of increasing: ♦ the strength of atrial contractions; ♦ total blood volume; ♦ venous tone (also increases venous return to the heart); ♦ pumping function of skeletal muscles (to move blood through the veins - as a result, the venous

Rice. 23-11. FRANK-STARLING MECHANISM. A. Scheme of the experiment(drug "heart-lung"). 1 - resistance control; 2 - compression chamber; 3 - reservoir; 4 - the volume of the ventricles. B. Inotropic effect

return; the pumping function of skeletal muscles always increases during muscular work); * negative intrathoracic pressure (venous return also increases). ❖ Stretching of cardiomyocytes decreases under the influence of: * vertical position of the body (due to a decrease in venous return); * increase in intrapericardial pressure; * reduce the compliance of the walls of the ventricles.

Influence of the sympathetic and vagus nerves on the pumping function of the heart

The efficiency of the pumping function of the heart is controlled by impulses from the sympathetic and vagus nerves. sympathetic nerves. Excitation of the sympathetic nervous system can increase the heart rate from 70 per minute to 200 and even up to 250. Sympathetic stimulation increases the force of contractions of the heart, thereby increasing the volume and pressure of the pumped blood. Sympathetic stimulation can increase the performance of the heart by 2-3 times in addition to the increase in cardiac output caused by the Frank-Starling effect (Fig. 23-11B). Brake-

The sympathetic nervous system can be used to reduce the pumping function of the heart. Normally, the sympathetic nerves of the heart are constantly tonically discharged, maintaining a higher (30% higher) level of cardiac performance. Therefore, if the sympathetic activity of the heart is suppressed, then, accordingly, the frequency and strength of heart contractions will decrease, which leads to a decrease in the level of pumping function by at least 30% below normal. Nervus vagus. Strong excitation of the vagus nerve can completely stop the heart for a few seconds, but then the heart usually "escaps" from the influence of the vagus nerve and continues to contract at a rarer frequency - 40% less than normal. Vagus nerve stimulation can reduce the force of heart contractions by 20-30%. The fibers of the vagus nerve are distributed mainly in the atria, and there are few of them in the ventricles, the work of which determines the strength of the contractions of the heart. This explains the fact that the influence of excitation of the vagus nerve affects more the decrease in heart rate than the decrease in the force of contractions of the heart. However, a noticeable decrease in heart rate, together with some weakening of the strength of contractions, can reduce the performance of the heart by up to 50% or more, especially when the heart is working with a heavy load.

systemic circulation

Blood vessels are a closed system in which blood continuously circulates from the heart to the tissues and back to the heart. systemic circulation, or systemic circulation includes all vessels that receive blood from the left ventricle and end in the right atrium. The vessels located between the right ventricle and the left atrium are pulmonary circulation, or small circle of blood circulation.

Structural-functional classification

Depending on the structure of the wall of the blood vessel in the vascular system, there are arteries, arterioles, capillaries, venules and veins, intervascular anastomoses, microvasculature and hematic barriers(eg, hematoencephalic). Functionally, vessels are divided into shock-absorbing(arteries) resistive(terminal arteries and arterioles), precapillary sphincters(terminal section of precapillary arterioles), exchange(capillaries and venules) capacitive(veins) shunting(arteriovenous anastomoses).

Physiological parameters of blood flow

Below are the main physiological parameters needed to characterize blood flow.

Systolic pressure is the maximum pressure reached in the arterial system during systole. Normally, systolic pressure in the systemic circulation is on average 120 mm Hg.

diastolic pressure- the minimum pressure that occurs during diastole in the systemic circulation averages 80 mm Hg.

pulse pressure. The difference between systolic and diastolic pressure is called pulse pressure.

mean arterial pressure(SBP) is tentatively estimated by the formula:

The average blood pressure in the aorta (90-100 mm Hg) gradually decreases as the arteries branch. In the terminal arteries and arterioles, the pressure drops sharply (up to 35 mm Hg on average), and then slowly decreases to 10 mm Hg. in large veins (Fig. 23-12A).

Cross-sectional area. The diameter of the aorta of an adult is 2 cm, the cross-sectional area is about 3 cm 2. Toward the periphery, the cross-sectional area of ​​arterial vessels slowly but progressively increases. At the level of arterioles, the cross-sectional area is about 800 cm 2, and at the level of capillaries and veins - 3500 cm 2. The surface area of ​​the vessels decreases significantly when the venous vessels join to form a vena cava with a cross-sectional area of ​​7 cm 2 .

Linear blood flow velocity inversely proportional to the cross-sectional area of ​​the vascular bed. Therefore, the average speed of blood movement (Fig. 23-12B) is higher in the aorta (30 cm / s), gradually decreases in small arteries and the smallest in capillaries (0.026 cm / s), the total cross section of which is 1000 times greater than in the aorta . The mean flow velocity again increases in the veins and becomes relatively high in the vena cava (14 cm/s), but not as high as in the aorta.

Volumetric blood flow velocity(usually expressed in milliliters per minute or liters per minute). The total blood flow in an adult at rest is about 5000 ml / min. Exactly this

Rice. 23-12. BP values(BUT) and linear blood flow velocity(B) in various segments of the vascular system

The amount of blood pumped out by the heart every minute is why it is also called cardiac output. The rate of blood circulation (blood circulation rate) can be measured in practice: from the moment of injection of the preparation of bile salts into the cubital vein until the sensation of bitterness appears on the tongue (Fig. 23-13A). Normally, the speed of blood circulation is 15 s.

vascular capacity. The size of the vascular segments determines their vascular capacity. Arteries contain about 10% of the total circulating blood (CBV), capillaries about 5%, venules and small veins about 54%, and large veins about 21%. The chambers of the heart hold the remaining 10%. Venules and small veins have a large capacity, making them an efficient reservoir capable of storing large volumes of blood.

Methods for measuring blood flow

Electromagnetic flowmetry is based on the principle of voltage generation in a conductor moving through a magnetic field, and the proportionality of the magnitude of the voltage to the speed of movement. Blood is a conductor, a magnet is located around the vessel, and the voltage, proportional to the volume of blood flow, is measured by electrodes located on the surface of the vessel.

Doppler uses the principle of the passage of ultrasonic waves through the vessel and the reflection of waves from moving erythrocytes and leukocytes. The frequency of the reflected waves changes - increases in proportion to the speed of the blood flow.

Measurement of cardiac output carried out by the direct Fick method and by the indicator dilution method. The Fick method is based on an indirect calculation of the minute volume of blood circulation by arteriovenous O 2 difference and determination of the volume of oxygen consumed by a person per minute. The indicator dilution method (radioisotope method, thermodilution method) uses the introduction of indicators into the venous system, followed by sampling from the arterial system.

Plethysmography. Information about the blood flow in the extremities is obtained using plethysmography (Fig. 23-13B). The forearm is placed in a chamber filled with water, connected to a device that records fluctuations in the volume of the liquid. Changes in limb volume, reflecting changes in the amount of blood and interstitial fluid, shift fluid levels and are recorded with a plethysmograph. If the venous outflow of the limb is turned off, then the fluctuations in the volume of the limb are a function of the arterial blood flow of the limb (occlusive venous plethysmography).

Physics of fluid movement in blood vessels

The principles and equations used to describe the motion of ideal fluids in tubes are often used to explain

Rice. 23-13. Determination of blood flow time(A) and plethysmography(B). one -

marker injection site; 2 - endpoint (language); 3 - volume recorder; 4 - water; 5 - rubber sleeve

behavior of blood in blood vessels. However, blood vessels are not rigid tubes, and blood is not an ideal liquid, but a two-phase system (plasma and cells), so the characteristics of blood circulation deviate (sometimes quite noticeably) from theoretically calculated ones.

laminar flow. The movement of blood in blood vessels can be represented as laminar (i.e. streamlined, with parallel flow of layers). The layer adjacent to the vascular wall is practically immobile. The next layer moves at a low speed, in the layers closer to the center of the vessel, the speed of movement increases, and in the center of the flow it is maximum. Laminar motion is maintained until a certain critical velocity is reached. Above the critical velocity, laminar flow becomes turbulent (vortex). Laminar motion is silent, turbulent motion generates sounds that, at the proper intensity, are audible with a stethophonendoscope.

turbulent flow. The occurrence of turbulence depends on the flow rate, vessel diameter and blood viscosity. The narrowing of the artery increases the speed of blood flow through the narrowing, creating turbulence and sounds below the narrowing. Examples of noises perceived over the wall of an artery are noises over an area of ​​narrowing of an artery caused by an atherosclerotic plaque, and Korotkoff's tones when measuring blood pressure. With anemia, turbulence is observed in the ascending aorta due to a decrease in blood viscosity, hence the systolic murmur.

Poiseuille formula. The relationship between fluid flow in a long narrow tube, fluid viscosity, tube radius and resistance is determined by the Poiseuille formula:

Since the resistance is inversely proportional to the fourth power of the radius, the blood flow and resistance in the body change significantly depending on small changes in the caliber of the vessels. For example, blood flow through vessels doubles when their radius increases by only 19%. When the radius is doubled, the resistance is reduced by 6% of the original level. These calculations make it possible to understand why organ blood flow is so effectively regulated by minimal changes in the lumen of arterioles and why variations in arteriole diameter have such a strong effect on systemic BP. Viscosity and resistance. The resistance to blood flow is determined not only by the radius of the blood vessels (vascular resistance), but also by the viscosity of the blood. Plasma is about 1.8 times more viscous than water. The viscosity of whole blood is 3-4 times higher than the viscosity of water. Therefore, blood viscosity is largely dependent on hematocrit, i.e. percentage of erythrocytes in the blood. In large vessels, an increase in hematocrit causes the expected increase in viscosity. However, in vessels with a diameter of less than 100 µm, i.e. in arterioles, capillaries and venules, the change in viscosity per unit change in hematocrit is much less than in large vessels.

❖ Changes in hematocrit affect the peripheral resistance, mainly of large vessels. Severe polycythemia (an increase in the number of red blood cells of varying degrees of maturity) increases peripheral resistance, increasing the work of the heart. In anemia, peripheral resistance is reduced, partly due to a decrease in viscosity.

❖ In the vessels, red blood cells tend to be located in the center of the current blood flow. Consequently, blood with a low hematocrit moves along the walls of the vessels. Branches extending from large vessels at right angles may receive a disproportionately smaller number of red blood cells. This phenomenon, called plasma slip, may explain the

the fact that the hematocrit of capillary blood is consistently 25% lower than in the rest of the body.

Critical pressure of closure of the vessel lumen. In rigid tubes, the relationship between pressure and flow rate of a homogeneous fluid is linear; in vessels, there is no such relationship. If the pressure in small vessels decreases, then the blood flow stops before the pressure drops to zero. This applies primarily to the pressure that propels erythrocytes through capillaries, the diameter of which is smaller than the size of erythrocytes. The tissues surrounding the vessels exert a constant slight pressure on them. When intravascular pressure falls below tissue pressure, the vessels collapse. The pressure at which blood flow stops is called the critical closure pressure.

Extensibility and compliance of blood vessels. All vessels are distensible. This property plays an important role in blood circulation. Thus, the extensibility of the arteries contributes to the formation of a continuous blood flow (perfusion) through the system of small vessels in the tissues. Of all the vessels, veins are the most extensible. A slight increase in venous pressure leads to the deposition of a significant amount of blood, providing a capacitive (accumulating) function of the venous system. Vascular compliance is defined as the increase in volume in response to an increase in pressure, expressed in millimeters of mercury. If the pressure is 1 mm Hg. causes an increase in this volume by 1 ml in a blood vessel containing 10 ml of blood, then the distensibility will be 0.1 per 1 mm Hg. (10% per 1 mmHg).

BLOOD FLOW IN ARTERIES AND ARTERIOLES

Pulse

Pulse - rhythmic fluctuations in the wall of the arteries, caused by an increase in pressure in the arterial system at the time of systole. During each systole of the left ventricle, a new portion of blood enters the aorta. This leads to stretching of the proximal aortic wall, since the inertia of the blood prevents the immediate movement of blood towards the periphery. The increase in pressure in the aorta quickly overcomes the inertia of the blood column, and the front of the pressure wave, stretching the wall of the aorta, spreads further and further along the arteries. This process is a pulse wave - the spread of pulse pressure through the arteries. The compliance of the arterial wall smooths out pulse fluctuations, gradually decreasing their amplitude towards the capillaries (Fig. 23-14B).

Rice. 23-14. arterial pulse. A. Sphygmogram. ab - anacrota; vg - systolic plateau; de - catacrot; g - notch (notch). . B. The movement of the pulse wave in the direction of small vessels. Decreased pulse pressure

Sphygmogram(Fig. 23-14A) On the pulse curve (sphygmogram) of the aorta, a rise is distinguished (anacrota), arising from the action of blood ejected from the left ventricle at the time of systole, and a decline (catacrotic) occurring at the time of diastole. A notch on a catacrot occurs due to the reverse movement of blood towards the heart at the moment when the pressure in the ventricle becomes lower than the pressure in the aorta and the blood rushes back along the pressure gradient towards the ventricle. Under the influence of the reverse flow of blood, the semilunar valves close, a wave of blood is reflected from the valves and creates a small secondary wave of pressure increase (dicrotic rise).

Pulse wave speed: aorta - 4-6 m/s, muscular arteries - 8-12 m/s, small arteries and arterioles - 15-35 m/s.

Pulse pressure- the difference between systolic and diastolic pressure - depends on the stroke volume of the heart and compliance of the arterial system. The greater the stroke volume and the more blood enters the arterial system during each heartbeat, the greater the pulse pressure. The lower the total peripheral vascular resistance, the greater the pulse pressure.

Decay of pulse pressure. The progressive decrease in pulsations in the peripheral vessels is called the attenuation of pulse pressure. The reasons for the weakening of pulse pressure are resistance to blood flow and vascular compliance. Resistance weakens the pulsation due to the fact that a certain amount of blood must move ahead of the front of the pulse wave to stretch the next segment of the vessel. The greater the resistance, the more difficulties arise. Compliance causes the pulse wave to decay because more compliant vessels require more blood ahead of the pulse wave front to cause an increase in pressure. In this way, the degree of attenuation of the pulse wave is directly proportional to the total peripheral resistance.

Blood pressure measurement

direct method. In some clinical situations, blood pressure is measured by inserting a needle with pressure sensors into the artery. This direct way definitions showed that blood pressure constantly fluctuates within the boundaries of a certain constant average level. On the records of the blood pressure curve, three types of oscillations (waves) are observed - pulse(coinciding with the contractions of the heart), respiratory(coinciding with respiratory movements) and intermittent slow(reflect fluctuations in the tone of the vasomotor center).

Indirect method. In practice, systolic and diastolic blood pressure is measured indirectly using the Riva-Rocci auscultatory method with the determination of Korotkoff sounds (Fig. 23-15).

Systolic BP. A hollow rubber chamber (located inside a cuff that can be fixed around the lower half of the shoulder), connected by a tube system with a rubber bulb and a pressure gauge, is placed on the shoulder. The stethoscope is placed over the anterior cubital artery in the cubital fossa. Inflating the cuff compresses the upper arm, and the reading on the pressure gauge registers the amount of pressure. The cuff placed on the upper arm is inflated until the pressure in it exceeds the level of systolic blood pressure, and then the air is slowly released from it. As soon as the pressure in the cuff is less than systolic, blood begins to break through the artery squeezed by the cuff - at the time of the peak of systolic blood pressure in the anterior ulnar artery, knocking tones begin to be heard, synchronous with heart beats. At this point, the pressure level of the manometer associated with the cuff indicates the value of systolic blood pressure.

Rice. 23-15. Blood pressure measurement

Diastolic BP. As the pressure in the cuff decreases, the nature of the tones changes: they become less knocking, more rhythmic and muffled. Finally, when the pressure in the cuff reaches the level of diastolic BP, the artery is no longer compressed during diastole - the tones disappear. The moment of their complete disappearance indicates that the pressure in the cuff corresponds to diastolic blood pressure.

Tones of Korotkov. The occurrence of Korotkoff's tones is due to the movement of a jet of blood through a partially compressed section of the artery. The jet causes turbulence in the vessel below the cuff, which causes vibrating sounds heard through the stethophonendoscope.

Error. With the auscultatory method for determining systolic and diastolic blood pressure, there may be discrepancies from the values ​​obtained by direct measurement of pressure (up to 10%). Automatic electronic blood pressure monitors, as a rule, underestimate the values ​​of both systolic and diastolic blood pressure by 10%.

Factors affecting blood pressure values

❖ Age. In healthy people, the value of systolic blood pressure increases from 115 mm Hg. at the age of 15 years up to 140 mm. Hg at the age of 65, i.e. an increase in blood pressure occurs at a rate of about 0.5 mm Hg. in year. Diastolic blood pressure increases from 70 mm Hg. at the age of 15 years up to 90 mm Hg, i.e. at a rate of about 0.4 mm Hg. in year.

❖ Floor. In women, systolic and diastolic BP are lower between the ages of 40 and 50, but higher between the ages of 50 and over.

❖ Body mass. Systolic and diastolic blood pressure are directly correlated with human body weight - the greater the body weight, the higher the blood pressure.

❖ Body position. When a person stands up, gravity alters venous return, decreasing cardiac output and blood pressure. Compensatory increases in heart rate, causing an increase in systolic and diastolic blood pressure and total peripheral resistance.

❖ Muscular activity. BP rises during work. Systolic blood pressure increases due to increased heart contractions. Diastolic blood pressure initially decreases due to vasodilatation of the working muscles, and then the intensive work of the heart leads to an increase in diastolic blood pressure.

VENOUS CIRCULATION

The movement of blood through the veins is carried out as a result of the pumping function of the heart. Venous blood flow also increases during each breath due to negative pressure in the chest cavity (suction action) and due to contractions of the skeletal muscles of the extremities (primarily the legs) that compress the veins.

Venous pressure

Central venous pressure- pressure in large veins at the place of their confluence with the right atrium - averages about 4.6 mm Hg. Central venous pressure is an important clinical characteristic necessary to assess the pumping function of the heart. At the same time, it is crucial pressure in the right atrium(about 0 mm Hg) - a regulator of the balance between the ability of the heart to pump blood from the right atrium and right ventricle to the lungs and the ability of blood to flow from peripheral veins to the right atrium (venous return). If the heart works intensively, then the pressure in the right ventricle decreases. On the contrary, the weakening of the work of the heart increases the pressure in the right atrium. Any influence that accelerates the flow of blood into the right atrium from the peripheral veins increases the pressure in the right atrium.

Peripheral venous pressure. The pressure in the venules is 12-18 mm Hg. It decreases in large veins to about 5.5 mm Hg, since in them the resistance to blood flow is reduced or practically absent. Moreover, in the thoracic and abdominal cavities, the veins are compressed by the surrounding structures.

Influence of intra-abdominal pressure. In the abdominal cavity in the supine position, the pressure is 6 mm Hg. It can rise from 15 to 30 mm. Hg during pregnancy, a large tumor, or the appearance of excess fluid in the abdominal cavity (ascites). In these cases, the pressure in the veins of the lower extremities becomes higher than intra-abdominal.

Gravity and venous pressure. At the surface of a body, the pressure of a liquid medium is equal to atmospheric pressure. The pressure in the body increases as you move deeper from the surface of the body. This pressure is the result of the action of the gravity of water, so it is called gravitational (hydrostatic) pressure. The effect of gravity on the vascular system is due to the weight of the blood in the vessels (Fig. 23-16A).

Rice. 23-16. VENOUS BLOOD FLOW. A. Effect of gravity on venous pressure in vertical position B. Venous(muscular) pump and the role of venous valves

Muscle pump and vein valves. The veins of the lower extremities are surrounded by skeletal muscles, the contractions of which compress the veins. The pulsation of neighboring arteries also exerts a compressive effect on the veins. Since the venous valves prevent the reverse movement, the blood moves towards the heart. As shown in fig. 23-16B, the valves of the veins are oriented to move blood towards the heart.

Suction action of heart contractions. Pressure changes in the right atrium are transmitted to large veins. Right atrial pressure drops sharply during the ejection phase of ventricular systole because the atrioventricular valves retract into the ventricular cavity, increasing atrial capacity. There is an absorption of blood into the atrium from large veins, and in the vicinity of the heart, venous blood flow becomes pulsating.

Depositing function of veins

More than 60% of the BCC is in the veins due to their high compliance. With a large blood loss and a drop in blood pressure, reflexes arise from the receptors of the carotid sinuses and other receptor vascular areas, activating the sympathetic nerves of the veins and causing their narrowing. This leads to the restoration of many reactions of the circulatory system, disturbed by blood loss. Indeed, even after the loss of 20% of the total blood volume, the circulatory system restores its normal functions due to the release of reserve blood volumes from the veins. In general, the specialized areas of blood circulation (the so-called "blood depot") include:

The liver, whose sinuses can release several hundred milliliters of blood into the circulation; ❖ spleen, capable of releasing up to 1000 ml of blood into the circulation, ❖ large abdominal veins, accumulating more than 300 ml of blood, ❖ subcutaneous venous plexus, capable of depositing several hundred milliliters of blood.

TRANSPORT OF OXYGEN AND CARBON DIOXIDE

Blood gas transport is discussed in Chapter 24. MICROCIRCULATION

The functioning of the cardiovascular system maintains the homeostatic environment of the body. The functions of the heart and peripheral vessels are coordinated to transport blood to the capillary network, where the exchange between blood and tissue is carried out.

liquid. The transfer of water and substances through the wall of blood vessels is carried out by diffusion, pinocytosis and filtration. These processes take place in a complex of vessels known as the microcirculatory unit. Microcirculatory unit consists of successively located vessels, these are terminal (terminal) arterioles - metarteriols - precapillary sphincters - capillaries - venules. In addition, arteriovenous anastomoses are included in the composition of microcirculatory units.

Organization and functional characteristics

Functionally, the vessels of the microvasculature are divided into resistive, exchange, shunt and capacitive.

Resistive vessels

❖ Resistive precapillary vessels: small arteries, terminal arterioles, metarterioles and precapillary sphincters. Precapillary sphincters regulate the functions of capillaries, being responsible for: ♦ the number of open capillaries;

♦ distribution of capillary blood flow, speed of capillary blood flow; ♦ effective surface of capillaries;

♦ average distance for diffusion.

❖ Resistive post-capillary vessels: small veins and venules containing SMC in their wall. Therefore, despite small changes in resistance, they have a noticeable effect on capillary pressure. The ratio of precapillary to postcapillary resistance determines the magnitude of capillary hydrostatic pressure.

exchange vessels. Efficient exchange between the blood and the extravascular environment occurs through the wall of capillaries and venules. The greatest intensity of exchange is observed at the venous end of the exchange vessels, because they are more permeable to water and solutions.

Shunt vessels- arteriovenous anastomoses and main capillaries. In the skin, shunt vessels are involved in the regulation of body temperature.

capacitive vessels- small veins with a high degree of compliance.

Blood flow speed. In arterioles, the blood flow velocity is 4-5 mm/s, in veins - 2-3 mm/s. Erythrocytes move through the capillaries one by one, changing their shape due to the narrow lumen of the vessels. The speed of movement of erythrocytes is about 1 mm / s.

Intermittent blood flow. The blood flow in an individual capillary depends primarily on the state of the precapillary sphincters and metatarsus.

riol, which periodically contract and relax. The period of contraction or relaxation can take from 30 seconds to several minutes. Such phase contractions are the result of the response of SMCs of vessels to local chemical, myogenic and neurogenic influences. The most important factor responsible for the degree of opening or closing of metarterioles and capillaries is the oxygen concentration in the tissues. If the oxygen content in the tissue decreases, then the frequency of intermittent periods of blood flow increases.

The rate and nature of transcapillary exchange depend on the nature of the transported molecules (polar or non-polar substances, see Chapter 2), the presence of pores and endothelial fenestres in the capillary wall, the endothelial basement membrane, and the possibility of pinocytosis through the capillary wall.

Transcapillary fluid movement is determined by the relationship between the capillary and interstitial hydrostatic and oncotic forces, first described by Starling, acting through the capillary wall. This movement can be described by the following formula:

V = K f x[(P - P 2) - (P3 - P 4)],

where V is the volume of liquid passing through the capillary wall in 1 min; K - filtration coefficient; P 1 - hydrostatic pressure in the capillary; P 2 - hydrostatic pressure in the interstitial fluid; P 3 - oncotic pressure in plasma; P 4 - oncotic pressure in the interstitial fluid. Capillary filtration coefficient (K f) - the volume of liquid filtered in 1 min 100 g of tissue with a change in pressure in the capillary of 1 mm Hg. K f reflects the state of hydraulic conductivity and the surface of the capillary wall.

Capillary hydrostatic pressure- the main factor in the control of transcapillary fluid movement - is determined by blood pressure, peripheral venous pressure, precapillary and postcapillary resistance. At the arterial end of the capillary, the hydrostatic pressure is 30-40 mm Hg, and at the venous end it is 10-15 mm Hg. An increase in arterial, peripheral venous pressure and post-capillary resistance or a decrease in pre-capillary resistance will increase capillary hydrostatic pressure.

Plasma oncotic pressure determined by albumins and globulins, as well as the osmotic pressure of electrolytes. Oncotic pressure throughout the capillary remains relatively constant, amounting to 25 mm Hg.

interstitial fluid formed by filtration from capillaries. The fluid composition is similar to that of blood plasma, except for the lower protein content. At short distances between capillaries and tissue cells, diffusion provides rapid transport through the interstitium of not only water molecules, but also electrolytes, nutrients with a small molecular weight, cellular metabolism products, oxygen, carbon dioxide and other compounds.

Hydrostatic pressure of the interstitial fluid ranges from -8 to +1 mm Hg. It depends on the volume of fluid and the compliance of the interstitial space (the ability to accumulate fluid without a significant increase in pressure). The volume of interstitial fluid is from 15 to 20% of the total body weight. Fluctuations in this volume depend on the ratio between inflow (filtration from capillaries) and outflow (lymph outflow). Compliance of the interstitial space is determined by the presence of collagen and the degree of hydration.

Oncotic pressure of the interstitial fluid determined by the amount of protein penetrating through the capillary wall into the interstitial space. The total amount of protein in 12 liters of interstitial body fluid is slightly greater than in the plasma itself. But since the volume of interstitial fluid is 4 times the volume of plasma, the protein concentration in the interstitial fluid is 40% of the protein content in plasma. On average, the colloid osmotic pressure in the interstitial fluid is about 8 mm Hg.

The movement of fluid through the capillary wall

The average capillary pressure at the arterial end of the capillaries is 15-25 mm Hg. more than at the venous end. Due to this pressure difference, blood is filtered from the capillary at the arterial end and reabsorbed at the venous end.

Arterial part of the capillary. The movement of fluid at the arterial end of the capillary determines the colloid osmotic pressure of the plasma (28 mm Hg, which contributes to the movement of fluid into the capillary) and the sum of forces (41 mm Hg) that move the fluid out of the capillary (pressure at the arterial end of the capillary is 30 mm Hg, negative interstitial pressure of the free fluid - 3 mm Hg, colloid osmotic pressure of the interstitial fluid - 8 mm Hg). The pressure difference between the outside and inside of the capillary is

Table 23-1. Fluid movement at the venous end of a capillary

13 mmHg These 13 mm Hg. constitute filter pressure, causing the transition of 0.5% of the plasma at the arterial end of the capillary into the interstitial space. The venous part of the capillary. In table. 23-1 shows the forces that determine the movement of fluid at the venous end of the capillary. Thus, the pressure difference between the inside and outside of the capillary (28 and 21) is 7 mmHg, which is reabsorption pressure at the venous end of the capillary. The low pressure at the venous end of the capillary changes the balance of forces in favor of absorption. The reabsorption pressure is significantly lower than the filtration pressure at the arterial end of the capillary. However, venous capillaries are more numerous and more permeable. The reabsorption pressure ensures that 9/10 of the fluid filtered at the arterial end is reabsorbed. The remaining fluid enters the lymphatic vessels.

lymphatic system

The lymphatic system is a network of vessels that return interstitial fluid to the blood (Fig. 23-17B).

Lymph formation

The volume of fluid returning to the bloodstream through the lymphatic system is 2 to 3 liters per day. Substances with a high molecular weight (especially proteins) cannot be absorbed from tissues in any other way, except for the lymphatic capillaries, which have a special structure.

Rice. 23-17. LYMPHATIC SYSTEM. A. Structure at the level of the microvasculature. B. Anatomy of the lymphatic system. B. Lymphatic capillary. 1 - blood capillary; 2 - lymphatic capillary; 3 - lymph nodes; 4 - lymphatic valves; 5 - precapillary arteriole; 6 - muscle fiber; 7 - nerve; 8 - venule; 9 - endothelium; 10 - valves; 11 - supporting filaments. D. Vessels of the microvasculature of the skeletal muscle. With the expansion of the arteriole (a), the lymphatic capillaries adjacent to it are compressed between it and the muscle fibers (above), with the narrowing of the arteriole (b), the lymphatic capillaries, on the contrary, expand (below). In skeletal muscle, blood capillaries are much smaller than lymphatic capillaries.

Lymph composition. Since 2/3 of the lymph comes from the liver, where the protein content exceeds 6 g per 100 ml, and the intestine, with a protein content above 4 g per 100 ml, the protein concentration in the thoracic duct is usually 3-5 g per 100 ml. After the

Ema fatty foods content of fats in the lymph of the thoracic duct can increase up to 2%. Through the wall of the lymphatic capillaries, bacteria can enter the lymph, which are destroyed and removed, passing through the lymph nodes.

The flow of interstitial fluid into the lymphatic capillaries(Fig. 23-17C,D). The endothelial cells of the lymphatic capillaries are fixed to the surrounding connective tissue by the so-called supporting filaments. At the contact points of endothelial cells, the end of one endothelial cell overlaps the edge of another cell. The overlapping edges of the cells form like valves protruding into the lymphatic capillary. These valves regulate the flow of interstitial fluid into the lumen of the lymphatic capillaries.

Ultrafiltration from lymphatic capillaries. The wall of the lymphatic capillary is a semi-permeable membrane, so some of the water is returned to the interstitial fluid by ultrafiltration. The colloid osmotic pressure of the fluid in the lymphatic capillary and interstitial fluid is the same, but the hydrostatic pressure in the lymphatic capillary exceeds that of the interstitial fluid, which leads to fluid ultrafiltration and lymph concentration. As a result of these processes, the concentration of proteins in the lymph increases by about 3 times.

Compression of the lymphatic capillaries. The movements of muscles and organs lead to compression of the lymphatic capillaries. In skeletal muscles, lymphatic capillaries are located in the adventitia of the precapillary arterioles (Fig. 23-17D). With the expansion of arterioles, the lymphatic capillaries are compressed between them and the muscle fibers, while the inlet valves are closed. When the arterioles constrict, the inlet valves, on the contrary, open, and the interstitial fluid enters the lymphatic capillaries.

Lymph movement

lymphatic capillaries. Lymph flow in the capillaries is minimal if the pressure of the interstitial fluid is negative (for example, less than - 6 mm Hg). An increase in pressure above 0 mm Hg. increases lymph flow by 20 times. Therefore, any factor that increases the pressure of the interstitial fluid also increases the lymph flow. Factors that increase interstitial pressure include: O increase

permeability of blood capillaries; O increase in colloid osmotic pressure of interstitial fluid; About the increase in pressure in the capillaries; О decrease in plasma colloid osmotic pressure.

Lymphangions. An increase in interstitial pressure is not enough to provide lymphatic flow against the forces of gravity. Passive mechanisms of lymph outflow- pulsation of the arteries, affecting the movement of lymph in the deep lymphatic vessels, contraction of skeletal muscles, movement of the diaphragm - cannot provide lymph flow in the vertical position of the body. This function is actively provided lymphatic pump. Segments of lymphatic vessels limited by valves and containing SMCs (lymphangions) in the wall are able to automatically contract. Each lymphangion functions as a separate automatic pump. Filling the lymphangion with lymph causes contraction, and the lymph is pumped through the valves to the next segment, and so on, until the lymph enters the bloodstream. In large lymphatic vessels (for example, in the thoracic duct), the lymphatic pump creates a pressure of 50 to 100 mmHg.

Thoracic ducts. At rest, up to 100 ml of lymph per hour passes through the thoracic duct, about 20 ml through the right lymphatic duct. Every day, 2-3 liters of lymph enter the bloodstream.

blood flow regulation mechanisms

Changes in pO 2 , pCO 2 in the blood, the concentration of H +, lactic acid, pyruvate and a number of other metabolites have local effects on the vessel wall and are recorded by chemoreceptors present in the vessel wall, as well as by baroreceptors that respond to pressure in the vessel lumen. These signals are received vasomotor center. The CNS implements responses motor autonomic innervation SMC of the walls of blood vessels and myocardium. In addition, there is a powerful humoral regulator system SMC of the vessel wall (vasoconstrictors and vasodilators) and endothelial permeability. Leading regulation parameter - systemic blood pressure.

Local regulatory mechanisms

Self-regulation. The ability of tissues and organs to regulate their own blood flow - self-regulation. Vessels of many organs

give the internal ability to compensate for moderate changes in perfusion pressure by changing vascular resistance in such a way that blood flow remains relatively constant. Self-regulatory mechanisms function in the kidneys, mesentery, skeletal muscles, brain, liver, and myocardium. Distinguish between myogenic and metabolic self-regulation.

Myogenic self-regulation. Self-regulation is partly due to the contractile response of SMCs to stretch, this is myogenic self-regulation. As soon as the pressure in the vessel begins to rise, the blood vessels stretch and the MMCs surrounding their wall contract.

Metabolic self-regulation. Vasodilator substances tend to accumulate in working tissues, which contributes to self-regulation, this is metabolic self-regulation. The decrease in blood flow leads to the accumulation of vasodilators (vasodilators) and the vessels dilate (vasodilation). When blood flow increases, these substances are removed, resulting in a situation of maintaining vascular tone. Vasodilating effects. The metabolic changes that cause vasodilation in most tissues are a decrease in pO 2 and pH. These changes lead to relaxation of the arterioles and precatillary sphincters. An increase in pCO 2 and osmolality also relaxes the vessels. The direct vasodilating effect of CO 2 is most pronounced in brain tissues and skin. An increase in temperature has a direct vasodilating effect. The temperature in the tissues as a result of increased metabolism increases, which also contributes to vasodilation. Lactic acid and K+ ions dilate the vessels of the brain and skeletal muscles. Adenosine dilates the vessels of the heart muscle and prevents the release of the vasoconstrictor norepinephrine.

Endothelial regulators

Prostacycline and thromboxane A 2 . Prostacyclin is produced by endothelial cells and promotes vasodilation. Thromboxane A 2 is released from platelets and promotes vasoconstriction.

Endogenous relaxing factor- nitric oxide (NO). Vascular endothelial cells under the influence of various substances and/or conditions synthesize the so-called endogenous relaxing factor (nitric oxide - NO). NO activates guanylate cyclase in cells, which is necessary for the synthesis of cGMP, which ultimately has a relaxing effect on the SMC of the vascular wall.

ki. Suppression of the function of NO-synthase markedly increases systemic blood pressure. At the same time, the erection of the penis is associated with the release of NO, which causes the expansion and filling of the cavernous bodies with blood.

Endothelins- 21-amino acid peptide s are represented by three isoforms. Endothelin 1 is synthesized by endothelial cells (especially the endothelium of veins, coronary arteries and cerebral arteries), it is a powerful vasoconstrictor.

The role of ions. The effect of increasing the concentration of ions in blood plasma on vascular function is the result of their action on the contractile apparatus of vascular smooth muscles. Particularly important is the role of Ca2+ ions, which cause vasoconstriction as a result of stimulation of MMC contraction.

CO 2 and vascular tone. Increasing the concentration of CO 2 in most tissues moderately dilates blood vessels, but in the brain the vasodilating effect of CO 2 is particularly pronounced. The effect of CO 2 on the vasomotor centers of the brainstem activates the sympathetic nervous system and causes general vasoconstriction in all areas of the body.

Humoral regulation of blood circulation

Biologically active substances circulating in the blood affect all parts of the cardiovascular system. Humoral vasodilating factors (vasodilators) include kinins, VIP, atrial natriuretic factor (atriopeptin), and humoral vasoconstrictors include vasopressin, norepinephrine, epinephrine, and angiotensin II.

Vasodilators

Kinina. Two vasodilatory peptides (bradykinin and kallidin - lysyl-bradykinin) are formed from precursor proteins - kininogens - under the action of proteases called kallikreins. Kinins cause: O contraction of the MMC of internal organs, O relaxation of the MMC of vessels and a decrease in blood pressure, O an increase in capillary permeability, O an increase in blood flow in the sweat and salivary glands and the exocrine part of the pancreas.

Atrial natriuretic factor atriopeptin: O increases the glomerular filtration rate, O reduces blood pressure, reducing the sensitivity of SMC vessels to the action of many vasoconstrictor substances; O inhibits the secretion of vasopressin and renin.

Vasoconstrictors

Norepinephrine and adrenaline. Norepinephrine is a powerful vasoconstrictor factor, adrenaline has a less pronounced vasoconstrictive effect, and in some vessels causes moderate vasodilation (for example, with increased myocardial contractile activity, adrenaline dilates the coronary arteries). Stress or muscle work stimulates the release of norepinephrine from sympathetic nerve endings in the tissues and has an exciting effect on the heart, causing narrowing of the lumen of the veins and arterioles. At the same time, the secretion of norepinephrine and adrenaline into the blood from the adrenal medulla increases. Acting in all areas of the body, these substances have the same vasoconstrictive effect on blood circulation as the activation of the sympathetic nervous system.

Angiotensins. Angiotensin II has a generalized vasoconstrictor effect. Angiotensin II is formed from angiotensin I (weak vasoconstrictor action), which, in turn, is formed from angiotensinogen under the influence of renin.

Vasopressin(antidiuretic hormone, ADH) has a pronounced vasoconstrictive effect. Vasopressin precursors are synthesized in the hypothalamus, transported along the axons to the posterior pituitary gland, and from there enter the bloodstream. Vasopressin also increases water reabsorption in the renal tubules.

Circulatory control by the nervous system

The basis of the regulation of the functions of the cardiovascular system is the tonic activity of the neurons of the medulla oblongata, the activity of which changes under the influence of afferent impulses from the sensitive receptors of the system - baro- and chemoreceptors. The vasomotor center of the medulla oblongata is subjected to stimulating influences from the overlying parts of the central nervous system with a decrease in the blood supply to the brain.

Vascular afferents

Baroreceptors especially numerous in the aortic arch and in the wall of large veins lying close to the heart. These nerve endings are formed by the terminals of the fibers passing through the vagus nerve.

Specialized sensory structures. The reflex regulation of blood circulation involves the carotid sinus and carotid body (Fig. 23-18B, 25-10A), as well as similar formations of the aortic arch, pulmonary trunk, and right subclavian artery.

O carotid sinus located near the bifurcation of the common carotid artery and contains numerous baroreceptors, the impulses from which enter the centers that regulate the activity of the cardiovascular system. The nerve endings of the baroreceptors of the carotid sinus are the terminals of the fibers passing through the sinus nerve (Hering) - a branch of the glossopharyngeal nerve.

O carotid body(Fig. 25-10B) responds to changes in the chemical composition of the blood and contains glomus cells that form synaptic contacts with the terminals of afferent fibers. Afferent fibers for the carotid body contain substance P and peptides related to the calcitonin gene. Glomus cells also end with efferent fibers passing through the sinus nerve (Hering) and postganglionic fibers from the superior cervical sympathetic ganglion. The terminals of these fibers contain light (acetylcholine) or granular (catecholamines) synaptic vesicles. The carotid body registers changes in pCO 2 and pO 2, as well as shifts in blood pH. Excitation is transmitted through synapses to afferent nerve fibers, through which impulses enter the centers that regulate the activity of the heart and blood vessels. Afferent fibers from the carotid body pass through the vagus and sinus nerves.

Vasomotor center

Groups of neurons located bilaterally in the reticular formation of the medulla oblongata and the lower third of the pons are united by the concept of "vasomotor center" (Fig. 23-18B). This center transmits parasympathetic influences via the vagus nerves to the heart and sympathetic influences via the spinal cord and peripheral sympathetic nerves to the heart and to all or almost all of the blood vessels. The vasomotor center includes two parts - vasoconstrictor and vasodilator centers.

Vessels. The vasoconstrictor center constantly transmits signals with a frequency of 0.5 to 2 Hz along the sympathetic vasoconstrictor nerves. This constant stimulation is referred to as Sim-

Rice. 23-18. CIRCULATION CONTROL FROM THE NERVOUS SYSTEM. A. Motor sympathetic innervation of blood vessels. B. Axon reflex. Antidromic impulses lead to the release of substance P, which dilates blood vessels and increases capillary permeability. B. Mechanisms of the medulla oblongata that control blood pressure. GL - glutamate; NA - norepinephrine; AH - acetylcholine; A - adrenaline; IX - glossopharyngeal nerve; X - vagus nerve. 1 - carotid sinus; 2 - aortic arch; 3 - baroreceptor afferents; 4 - inhibitory intercalary neurons; 5 - bulbospinal path; 6 - sympathetic preganglionic; 7 - sympathetic postganglionic; 8 - the core of a single path; 9 - rostral ventrolateral nucleus

pathic vasoconstrictor tone, and the state of constant partial contraction of the SMC of blood vessels - vasomotor tone.

Heart. At the same time, the vasomotor center controls the activity of the heart. The lateral sections of the vasomotor center transmit excitatory signals through the sympathetic nerves to the heart, increasing the frequency and strength of its contractions. The medial sections of the vasomotor center transmit parasympathetic impulses through the motor nuclei of the vagus nerve and fibers of the vagus nerves, which slow down the heart rate. The frequency and force of contractions of the heart increase simultaneously with the constriction of the vessels of the body and decrease simultaneously with the relaxation of the vessels.

Influences acting on the vasomotor center: O direct stimulation(CO 2 , hypoxia);

O exciting influences nervous system from the cerebral cortex through the hypothalamus, from pain receptors and muscle receptors, from the chemoreceptors of the carotid sinus and aortic arch.

O inhibitory influences nervous system from the cerebral cortex through the hypothalamus, from the lungs, from the baroreceptors of the carotid sinus, aortic arch and pulmonary artery.

Innervation of blood vessels

All blood vessels containing SMCs in their walls (i.e., with the exception of capillaries and some venules) are innervated by motor fibers from the sympathetic division of the autonomic nervous system. Sympathetic innervation of small arteries and arterioles regulates tissue blood flow and blood pressure. Sympathetic fibers innervating the venous capacitance vessels control the volume of blood deposited in the veins. Narrowing of the lumen of the veins reduces venous capacity and increases venous return.

Noradrenergic fibers. Their effect is to narrow the lumen of the vessels (Fig. 23-18A).

Sympathetic vasodilating nerve fibers. The resistive vessels of the skeletal muscles, in addition to the vasoconstrictor sympathetic fibers, are innervated by vasodilating cholinergic fibers passing through the sympathetic nerves. The blood vessels of the heart, lungs, kidneys, and uterus are also innervated by sympathetic cholinergic nerves.

Innervation of the MMC. Bundles of noradrenergic and cholinergic nerve fibers form plexuses in the adventitial sheath of arteries and arterioles. From these plexuses, varicose nerve fibers are directed to the muscular membrane and terminate in

its outer surface, without penetrating to the deeper MMCs. The neurotransmitter reaches the inner parts of the muscular membrane of the vessels by diffusion and propagation of excitation from one SMC to another through gap junctions.

Tone. Vasodilating nerve fibers are not in a state of constant excitation (tonus), while vasoconstrictor fibers, as a rule, exhibit tonic activity. If the sympathetic nerves are cut (which is referred to as a sympathectomy), then the blood vessels dilate. In most tissues, vasodilation results from a reduction in the frequency of tonic discharges in vasoconstrictor nerves.

Axon reflex. Mechanical or chemical irritation of the skin may be accompanied by local vasodilation. It is believed that when irritating thin, non-myelinated skin pain fibers, AP propagate not only in the centripetal direction to the spinal cord (orthodromous), but also by efferent collaterals (antidromic) they enter the blood vessels of the area of ​​the skin innervated by this nerve (Fig. 23-18B). This local neural mechanism is called the axon reflex.

Blood pressure regulation

BP is maintained at the required working level with the help of reflex control mechanisms that operate on the basis of the feedback principle.

baroreceptor reflex. One of the well-known neural mechanisms for controlling blood pressure is the baroreceptor reflex. Baroreceptors are present in the wall of almost all large arteries in the chest and neck, especially many baroreceptors in the carotid sinus and in the wall of the aortic arch. The baroreceptors of the carotid sinus (see Figure 25-10) and the aortic arch do not respond to blood pressure in the range from 0 to 60-80 mm Hg. An increase in pressure above this level causes a response, which progressively increases and reaches a maximum at a blood pressure of about 180 mm Hg. Normal blood pressure (its systolic level) ranges from 110-120 mm Hg. Small deviations from this level increase the excitation of baroreceptors. Baroreceptors respond to changes in blood pressure very quickly: the frequency of impulses increases during systole and decreases just as quickly during diastole, which occurs within a fraction of a second. Thus, baroreceptors are more sensitive to changes in pressure than to its stable level.

O Increased impulses from baroreceptors, caused by a rise in blood pressure, enters the medulla oblongata, inhibits the vasoconstrictor center of the medulla oblongata and excites the center of the vagus nerve. As a result, the lumen of the arterioles expands, the frequency and strength of heart contractions decrease. In other words, excitation of baroreceptors reflexively leads to a decrease in blood pressure due to a decrease in peripheral resistance and cardiac output.

O Low blood pressure has the opposite effect, which leads to its reflex increase to a normal level. A decrease in pressure in the carotid sinus and aortic arch inactivates baroreceptors, and they cease to have an inhibitory effect on the vasomotor center. As a result, the latter is activated and causes an increase in blood pressure.

Chemoreceptors in the carotid sinus and aorta. Chemoreceptors - chemosensitive cells that respond to a lack of oxygen, an excess of carbon dioxide and hydrogen ions - are located in the carotid bodies and in the aortic bodies. Chemoreceptor nerve fibers from the bodies, together with baroreceptor fibers, go to the vasomotor center of the medulla oblongata. When blood pressure drops below a critical level, chemoreceptors are stimulated, since the decrease in blood flow reduces the content of O 2 and increases the concentration of CO 2 and H +. Thus, impulses from chemoreceptors excite the vasomotor center and contribute to an increase in blood pressure.

Reflexes from the pulmonary artery and atria. In the wall of both atria and the pulmonary artery there are stretch receptors (low pressure receptors). Low pressure receptors perceive changes in volume that occur simultaneously with changes in blood pressure. Excitation of these receptors causes reflexes in parallel with baroreceptor reflexes.

Atrial reflexes activating the kidneys. Stretching of the atria causes a reflex expansion of the afferent (bringing) arterioles in the glomeruli of the kidneys. At the same time, a signal is sent from the atrium to the hypothalamus, reducing the secretion of ADH. The combination of two effects - an increase in glomerular filtration rate and a decrease in fluid reabsorption - contributes to a decrease in blood volume and its return to normal levels.

Atrial reflex that controls heart rate. An increase in pressure in the right atrium causes a reflex increase in heart rate (Bainbridge reflex). Atrial stretch receptors

evoking the Bainbridge reflex, transmit afferent signals through the vagus nerve to the medulla oblongata. Then the excitation returns back to the heart along the sympathetic pathways, increasing the frequency and strength of the contractions of the heart. This reflex prevents the veins, atria, and lungs from overflowing with blood. Arterial hypertension. Normal systolic/diastolic blood pressure is 120/80 mmHg. Arterial hypertension is a condition when systolic pressure exceeds 140 mm Hg, and diastolic - 90 mm Hg.

Heart rate control

Almost all mechanisms that control systemic blood pressure, in one way or another, change the rhythm of the heart. Stimuli that increase the heart rate also increase blood pressure. Stimuli that decrease the heart rate lower blood pressure. There are also exceptions. Thus, stimulation of atrial stretch receptors increases heart rate and causes arterial hypotension, and an increase in intracranial pressure causes bradycardia and an increase in blood pressure. In total increase heart rate decrease in activity of baroreceptors in the arteries, left ventricle and pulmonary artery, increase in activity of atrial stretch receptors, inhalation, emotional arousal, pain stimuli, muscle load, norepinephrine, adrenaline, thyroid hormones, fever, Bainbridge reflex and a sense of rage, and slow down the rhythm heart increase in the activity of baroreceptors in the arteries, left ventricle and pulmonary artery; expiration, irritation of the pain fibers of the trigeminal nerve and an increase in intracranial pressure.

conduction system of the heart. Innervation of the heart.

An important role in the rhythmic work of the heart and in the coordination of the activity of the muscles of the individual chambers of the heart is played by conducting system of the heart , which is a complex neuromuscular formation. The muscle fibers that make up its composition (conductive fibers) have a special structure: their cells are poor in myofibrils and rich in sarcoplasm, therefore they are lighter. They are sometimes visible to the naked eye in the form of light-colored threads and represent a less differentiated part of the original syncytium, although they are larger than ordinary muscle fibers of the heart. In a conducting system, nodes and bundles are distinguished.

1. sinoatrial node , nodus sinuatrialis, is located in the wall of the right atrium (in sulcus terminalis, between the superior vena cava and the right ear). It is associated with the muscles of the atria and is important for their rhythmic contraction.

2. atrioventricular node , nodus atrioventricularis, is located in the wall of the right atrium, near the cuspis septalis of the tricuspid valve. The fibers of the node, directly connected with the muscles of the atrium, continue into the septum between the ventricles in the form of an atrioventricular bundle, fasciculus atrioventricularis (bundle of His) . In the ventricular septum, the bundle divides into two legs - crus dextrum et sinistrum, which go into the walls of the same ventricles and branch under the endocardium in their muscles. The atrioventricular bundle is very important for the work of the heart, since a contraction wave is transmitted through it from the atria to the ventricles, due to which the regulation of the systole rhythm - the atria and ventricles - is established.

Therefore, the atria are connected to each other by the sinoatrial node, and the atria and ventricles are connected by the atrioventricular bundle. Usually, irritation from the right atrium is transmitted from the sinoatrial node to the atrioventricular node, and from it along the atrioventricular bundle to both ventricles.

The nerves that provide innervation to the cardiac muscles, which have a special structure and function, are complex and form numerous plexuses. The entire nervous system is composed of: 1) suitable trunks, 2) extracardiac plexuses, 3) plexuses in the heart itself, and 4) nodal fields associated with the plexus.

Functionally, the nerves of the heart are divided into 4 types (I.P. Pavlov): slowing down and accelerating, weakening and strengthening . Morphologically, these nerves go in n. vagus and branches truncus sympathicus. Sympathetic nerves (mainly postganglionic fibers) depart from the three upper cervical and five upper thoracic sympathetic nodes: n. cardiacus cervicalis superior, medius et inferior and nn. cardiaci thoracici from the thoracic nodes of the sympathetic trunk.

heart branches vagus nerve start from its cervical (rami cardiaci cervicales superiores), chest (rami cardiaci thoracici) and from n. laryngeus recurrens vagi (rami cardiaci cervicales inferiores). Nerves approaching the heart are divided into two groups - superficial and deep. Two nerve plexuses are formed from the listed sources:

1) superficial, plexus cardiacus superficialis, between the aortic arch (below it) and the bifurcation of the pulmonary trunk;

2) deep, plexus cardiacus profundus, between the aortic arch (behind it) and the bifurcation of the trachea.

These plexuses continue into the plexus coronarius dexter et sinister surrounding the vessels of the same name, as well as into the plexus located between the epicardium and myocardium. From the last plexus depart intraorgan branching of the nerves. The plexuses contain numerous groups of ganglion cells, nerve nodes.

Afferent fibers start from receptors and go together with efferent fibers as part of the vagus and sympathetic nerves.

The innervation of the heart is carried out by cardiac nerves that go as part of n. vagus and tr. sympathicus.
Sympathetic nerves depart from the three upper cervical and five upper thoracic sympathetic nodes: n. cardiacus cervicalis superior - from ganglion cervicale superius, n. cardiacus cervicalis medius - from ganglion cervicale medium, n. cardiacus cervicalis inferior - from ganglion cervicothoracicum (ganglion stellatum) and nn. cardiaci thoracici - from the thoracic nodes of the sympathetic trunk.
The cardiac branches of the vagus nerve start from its cervical region (rami cardiaci superiores). thoracic (rami cardiaci medii) and from n. laryngeus recurrens vagi (rami cardiaci inferiores). The entire complex of nerve branches forms extensive aortic and cardiac plexuses. Branches depart from them, forming the right and left coronary plexuses.
The regional lymph nodes of the heart are the tracheobronchial and paratracheal nodes. In these nodes there are paths for the outflow of lymph from the heart, lungs and esophagus.

Ticket number 60

1. Muscles of the foot. Functions, blood supply, innervation.

Dorsal muscles of the foot.

M. extensor digitorum brevis, a short extensor of the fingers, is located on the back of the foot under the tendons of the long extensor and originates on the calcaneus before entering the sinus tarsi. Heading forward, it is divided into four thin tendons to the I-IV fingers, which join the lateral edge of the tendons m. extensor digitorum longus and so on. extensor hallucis longus and together with them form the dorsal tendon sprain of the fingers. The medial abdomen, which goes obliquely along with its tendon to the thumb, also has a separate name m. extensor hallucis brevis.
Function. Makes the extension of the I-IV fingers along with their easy abduction to the lateral side. (Inn. LIV - “St. N. peroneus profundus.)

Plantar muscles of the foot.

They form three groups: medial (muscles of the thumb), lateral (muscles of the little finger) and middle, lying in the middle of the sole.

a) There are three muscles of the medial group:
1. M. abductor hallucis, the muscle that removes the big toe, is located most superficially on the medial edge of the sole; originates from the processus medialis of the calcaneal tubercle, retinaculum mm. flexdrum and tiberositas ossis navicularis; attaches to the medial sesamoid bone and the base of the proximal phalanx. (Inn. Lv - Sh N. plantaris med.).
2. M. flexor hallucis brevis, a short flexor of the big toe, adjacent to the lateral edge of the previous muscle, begins on the medial sphenoid bone and on the lig. calcaneocuboideum plantare. Going straight ahead, the muscle is divided into two heads, between which the tendon m passes. flexor hallucis longus. Both heads are attached to the sesamoid bones in the region of the first metatarsophalangeal articulation and to the base of the proximal phalanx of the thumb. (Inn. 5i_n. Nn. plantares medialis et lateralis.)
3. M. adductor hallucis, the muscle that leads the big toe, lies deep and consists of two heads. One of them (oblique head, caput obliquum) originates from the cuboid bone and lig. plantare longum, as well as from the lateral sphenoid and from the bases of the II-IV metatarsal bones, then goes obliquely forward and somewhat medially. Another head (transverse, caput transversum) gets its origin from the articular bags II-V metatarsophalangeal joints and plantar ligaments; it runs transversely to the length of the foot and, together with the oblique head, is attached to the lateral sesamoid bone of the thumb. (Inn. Si-ts. N. plantaris lateralis.)
Function. The muscles of the medial group of the sole, in addition to the actions indicated in the names, are involved in strengthening the arch of the foot on its medial side.

b) The muscles of the lateral group are among the two:
1. M. abductor digiti minimi, the muscle that abducts the little toe of the foot, lies along the lateral edge of the sole, more superficial than other muscles. It originates from the calcaneus and inserts at the base of the proximal phalanx of the little finger.
2. M. flexor digiti minimi brevis, a short flexor of the little toe of the foot, starts from the base of the fifth metatarsal bone and is attached to the base of the proximal phalanx of the little toe.
The function of the muscles of the lateral group of the sole in terms of the impact of each of them on the little finger is insignificant. Their main role is to strengthen the lateral edge of the arch of the foot. (Inn. of all three muscles 5i_n. N. plantaris lateralis.)

c) Muscles of the middle group:
1. M. flexor digitorum brevis, a short flexor of the fingers, lies superficially under the plantar aponeurosis. It starts from the calcaneal tuber and is divided into four flat tendons, attached to the middle phalanges of the II-V fingers. Before their attachment, the tendons are each split into two legs, between which the tendons m pass. flexor digitorum longus. The muscle fastens the arch of the foot in the longitudinal direction and flexes the toes (II-V). (Inn. Lw-Sx. N. plantaris medialis.)
2. M. quadrdtus plantae (m. flexor accessorius), the square muscle of the sole, lies under the previous muscle, starts from the calcaneus and then joins the lateral edge of the tendon m. flexor digitorum longus. This bundle regulates the action of the long flexor of the fingers, giving its thrust a direct direction in relation to the fingers. (Inn. 5i_u. N. plantaris lateralis.)
3. mm. lumbricales, worm-like muscles, four in number. As on the hand, they depart from; four tendons of the long flexor of the fingers and are attached to the medial edge of the proximal phalanx of the II-V fingers. They can flex the proximal phalanges; their extensor action on other phalanges is very weak or completely absent. They can still pull four other fingers towards the thumb. (Inn. Lv - Sn. Nn. plantares lateralis et medialis.)
4. mm. interossei, interosseous muscles, lie most deeply on the side of the sole, corresponding to the spaces between the metatarsal bones. Dividing, like the similar muscles of the hand, into two groups - three plantar, tt. interossei plantares, and four rear ones, vols. interossei dorsdles, at the same time they differ in their location. In the hand, in connection with its grasping function, they are grouped around the third finger; in the foot, in connection with its supporting role, they are grouped around the second finger, i.e., in relation to the second metatarsal bone. Functions: adduct and spread fingers, but in a very limited size. (Inn. 5i_n. N. plantaris lateralis.)

Blood supply: The foot receives blood from two arteries: the anterior and posterior tibial. The anterior tibial artery runs, as the name implies, in front of the foot and forms an arc on its rear. The posterior tibial artery runs on the sole and divides into two branches there. Blood supply:
Venous outflow from the foot is carried out through two superficial veins: large and small subcutaneous, and two deep, which go along the same arteries.

2. Anastomoses of arteries and anastomoses of veins. Ways of roundabout (collateral) blood flow (examples). Characteristics of the microcirculatory bed.
Anastomoses - connections between vessels - are subdivided among blood vessels into arterial, venous, arteriolo-venular. They can be intersystemic, when vessels belonging to different arteries or veins are connected; intrasystemic, when arterial or venous branches related to one artery or vein anastomose with each other. Both those and others are able to provide a roundabout, bypass (collateral) path of blood flow both in different functional states, and in case of blockage or ligation of the blood supply source.

The arterial circle of the brain is located at the base of the brain and is formed by the posterior cerebral arteries from the basilar and vertebral arteries of the subclavian system, the anterior and middle cerebral arteries from the internal carotid (the system of common carotid arteries). In a circle, the cerebral arteries connect the anterior and posterior connecting branches. Around and inside the thyroid gland, intersystemic anastomoses are formed between the superior thyroid arteries from the external carotid and the inferior thyroid arteries from the thyroid trunk of the subclavian artery. Intrasystemic anastomoses on the face occur in the region of the medial angle of the eye, where the angular branch of the facial artery from the external carotid connects with the dorsal artery of the nose - a branch of the ophthalmic artery from the internal carotid.

In the walls of the chest and abdomen, anastomoses occur between the posterior intercostal and lumbar arteries from the descending aorta, between the anterior intercostal branches of the internal thoracic artery (from the subclavian) and the posterior intercostal arteries from the aorta; between the superior and inferior epigastric arteries; between the superior and inferior phrenic arteries. There are also many organ connections, for example, between the arteries of the abdominal part of the esophagus and the left gastric, between the upper and lower pancreatoduodenal arteries and their branches in the pancreas, between the middle colon artery from the superior mesenteric and the left colon from the inferior mesenteric, between the adrenal arteries, between rectal arteries.

In the region of the upper shoulder girdle, an arterial scapular circle is formed due to the suprascapular (from the thyroid trunk) and circumflex scapular artery (from the axillary). Around the elbow and wrist joints are arterial networks of collateral and recurrent arteries. On the hand, the superficial and deep arterial arches are interconnected by palmar, dorsal and interosseous arteries. In the genital, gluteal regions and around the hip joint, anastomoses are formed between the iliac and femoral arteries, thanks to the iliac-lumbar, deep surrounding iliac, obturator, and gluteal arteries. The recurrent tibial and popliteal medial and lateral arteries form the network of the knee joint, and the ankle arteries form the network of the ankle joint. On the sole, deep plantar branches are connected with the plantar arch using the lateral plantar artery.

Between the superior and inferior vena cava, caval-caval anastomoses arise due to the epigastric (upper and lower veins) in the anterior abdominal wall, with the help of the vertebral venous plexus, unpaired, semi-unpaired, lumbar and posterior intercostal, diaphragmatic veins - in the posterior and upper walls of the abdomen. Between the hollow and portal veins, porto-caval anastomoses are formed due to the veins of the esophagus and stomach, rectum, adrenal glands, paraumbilical veins and others. The connections of the paraumbilical veins from the system of the portal vein of the liver with the supra- and hypogastric veins from the system of the vena cava become so noticeable in cirrhosis of the liver that they have received the expressive name "jellyfish head".

Venous plexuses of organs: vesical, utero-vaginal, rectal also represent one of the types of venous anastomoses. On the head, superficial veins, diploic veins of the skull, and sinuses of the dura mater are anastomosed with the help of emissary veins (veins of the graduate).

microcirculation.
The circulatory system consists of a central organ - the heart - and closed tubes of various calibers connected to it, called blood vessels. The blood vessels that lead from the heart to the organs and carry blood to them are called arteries. As they move away from the heart, the arteries divide into branches and become smaller and smaller. The arteries closest to the heart (the aorta and its large branches) are the main vessels, which mainly perform the function of conducting blood. In them, resistance to stretching with a mass of blood comes to the fore, therefore, in all three membranes (tunica intima, tunica media and tunica externa), mechanical structures are relatively more developed - elastic fibers, therefore such arteries are called arteries of the elastic type. In medium and small arteries, their own contraction of the vascular wall is required for the further movement of blood; they are characterized by the development of muscle tissue in the vascular wall - these are muscle-type arteries. In relation to the organ, there are arteries that go outside the organ - extraorganic and their continuations, branching inside it - intraorganic or intraorganic. The last branches of the arteries are arteroiles, its wall, unlike the artery, has only one layer of muscle cells, due to which they perform a regulatory function. The arteriole continues directly into the precapillary, from which numerous capillaries depart, performing an exchange function. Their wall consists of a single layer of flat endothelial cells.

Widely anastomosing with each other, the capillaries form networks that pass into postcapillaries, which continue into venules, they give rise to veins. Veins carry blood from organs to the heart. Their walls are much thinner than those of arteries. They have less elastic and muscle tissue. The movement of blood is carried out due to the activity and suction action of the heart and chest cavity, due to the pressure difference in the cavities and the contraction of the visceral and skeletal muscles. The reverse flow of blood is prevented by valves consisting of the endothelial wall. Arteries and veins usually go together, small and medium arteries are accompanied by two veins, and large ones by one. That. all blood vessels are divided into heart vessels - they begin and end both circles of blood circulation (aorta and pulmonary trunk), the main ones - serve to distribute the cut throughout the body. These are large and medium extraorganic arteries of the muscular type and extraorganic veins; organ - provide exchange reactions between the blood and the parenchyma of organs. These are intraorgan arteries and veins, as well as links of the microvasculature.

3. Gallbladder. Excretory ducts of the gallbladder and liver, blood supply, innervation.
Vesica fellea s. biliaris, the gallbladder is pear-shaped. Its wide end, which extends somewhat beyond the lower edge of the liver, is called the bottom, fundus vesicae felleae. The opposite narrow end of the gallbladder is called the neck, collum vesicae felleae; the middle part forms the body, corpus vesicae felleae.
The neck continues directly into the cystic duct, ductus cysticus, about 3.5 cm long. From the confluence of ductus cysticus and ductus hepaticus communis, a common bile duct is formed, ductus choledochus, bile duct (from the Greek dechomai - I accept). The latter lies between two sheets of lig. hepatoduodenale, having a portal vein behind it, and on the left - a common hepatic artery; then it goes down behind the upper part of the duodeni, pierces the medial wall of the pars descendens duodeni and opens along with the pancreatic duct with an opening into the extension located inside the papilla duodeni major and called ampulla hepatopancreatica. At the confluence of the duodenum ductus choledochus, the circular layer of the muscles of the duct wall is significantly strengthened and forms the so-called sphincter ductus choledochi, which regulates the flow of bile into the intestinal lumen; in the region of the ampulla there is another sphincter, m. sphincter ampullae hepatopancreaticae. The length of the ductus choledochus is about 7 cm.
The gallbladder is covered with peritoneum only from the lower surface; its bottom is adjacent to the anterior abdominal wall in the corner between the right m. rectus abdominis and the lower edge of the ribs. The muscular layer lying under the serous membrane, tunica muscularis, consists of involuntary muscle fibers with an admixture of fibrous tissue. The mucous membrane forms folds and contains many mucous glands. In the neck and in the ductus cysticus there are a number of folds arranged spirally and constituting a spiral fold, plica spiralis.

Innervation: The innervation of the gallbladder is carried out mainly by the anterior hepatic plexus, passing into this area from the perivascular plexuses of the hepatic and cystic arteries. Branches n. phrenicus provide afferent innervation of the gallbladder.
Blood supply: carried out by the cystic artery (a.cystica), which originates from the right hepatic artery (a.hepatica).
The outflow of venous blood from the gallbladder is carried out through the cystic veins. They are usually small in size, there are quite a few of them. The cystic veins collect blood from the deep layers of the gallbladder wall and enter the liver through the gallbladder bed. But in the cystic veins, blood flows into the hepatic vein system, and not the portal. The veins of the lower part of the common bile duct carry blood to the portal vein system.