How does nervous humoral regulation of the heart occur? The concept of nervous and humoral regulation of the activity of the heart

Factors of humoral regulation are divided into two groups:

1) substances of systemic action;

To systemic substances include electrolytes and hormones. Electrolytes (Ca ions) have a pronounced effect on the work of the heart (positive inotropic effect). With an excess of Ca, cardiac arrest can occur at the time of systole, since there is no complete relaxation. Na ions are able to have a moderate stimulating effect on the activity of the heart. With an increase in their concentration, a positive bathmotropic and dromotropic effect is observed. K ions in high concentrations have an inhibitory effect on the work of the heart due to hyperpolarization. However, a slight increase in K content stimulates coronary blood flow. It has now been found that with an increase in the level of K compared to Ca, a decrease in the work of the heart occurs, and vice versa.

The hormone adrenaline increases the strength and frequency of heart contractions, improves coronary blood flow and increases metabolic processes in the myocardium.

thyroxine (a hormone thyroid gland) enhances the work of the heart, stimulates metabolic processes, increases the sensitivity of the myocardium to adrenaline.

Mineralocorticoids (aldosterone) stimulate Na reabsorption and K excretion from the body.

Glucagon raises blood glucose levels by breaking down glycogen, resulting in a positive inotropic effect.

Sex hormones in relation to the activity of the heart are synergists and enhance the work of the heart.

Substances of local action operate where they are produced. These include mediators. For example, acetylcholine has five types of negative effects on the activity of the heart, and norepinephrine - on the contrary. Tissue hormones (kinins) are substances that have a high biological activity, but they are quickly destroyed, and therefore have a local effect. These include bradykinin, kalidin, moderately stimulating vessels. However, at high concentrations, they can cause a decrease in heart function. Prostaglandins, depending on the type and concentration, can have different effects. Metabolites formed during metabolic processes improve blood flow.

Thus, humoral regulation ensures a longer adaptation of the activity of the heart to the needs of the body.

10. Vascular tone and its regulation

Vascular tone, depending on the origin, can be myogenic and nervous.

Myogenic tone occurs when certain vascular smooth muscle cells begin to spontaneously generate a nerve impulse. The resulting excitation spreads to other cells, and contraction occurs. The tone is maintained by the basal mechanism. Different vessels have different basal tone: the maximum tone is observed in coronary vessels, skeletal muscles, kidneys, and the minimum - in the skin and mucous membranes. Its significance lies in the fact that vessels with a high basal tone on severe irritation respond with relaxation, and with low - contraction.

The nervous mechanism occurs in the smooth muscle cells of the vessels under the influence of impulses from the central nervous system. Due to this, there is an even greater increase in basal tone. Such a total tone is the resting tone, with a pulse frequency of 1–3 per second.

Thus, the vascular wall is in a state of moderate tension - vascular tone.

Currently, there are three mechanisms of regulation of vascular tone - local, nervous, humoral.

autoregulation provides a change in tone under the influence of local excitation. This mechanism is associated with relaxation and is manifested by the relaxation of smooth muscle cells. There is myogenic and metabolic autoregulation.

Myogenic regulation is associated with a change in the state of smooth muscles - this is the Ostroumov-Beilis effect, aimed at maintaining a constant level of blood volume supplied to the organ.

Metabolic regulation provides a change in the tone of smooth muscle cells under the influence of substances necessary for metabolic processes and metabolites. It is caused mainly by vasodilating factors:

1) lack of oxygen;

2) an increase in the content of carbon dioxide;

3) an excess of K, ATP, adenine, cATP.

Metabolic regulation is most pronounced in the coronary vessels, skeletal muscles, lungs, and brain. Thus, the mechanisms of autoregulation are so pronounced that in the vessels of some organs they offer maximum resistance to the constricting effect of the CNS.

Nervous regulation It is carried out under the influence of the autonomic nervous system, which acts as a vasoconstrictor and a vasodilator. Sympathetic nerves cause a vasoconstrictive effect in those in which β 1 -adrenergic receptors predominate. These are the blood vessels of the skin, mucous membranes, gastrointestinal tract. Impulses along the vasoconstrictor nerves arrive both at rest (1–3 per second) and in the state of activity (10–15 per second).

Vasodilating nerves can be of various origins:

1) parasympathetic nature;

2) sympathetic nature;

3) axon reflex.

The parasympathetic division innervates the vessels of the tongue, salivary glands, pia mater, external genitalia. The mediator acetylcholine interacts with M-cholinergic receptors vascular wall, which leads to expansion.

The sympathetic department is characterized by innervation of the coronary vessels, vessels of the brain, lungs, and skeletal muscles. This is due to the fact that adrenergic nerve endings interact with β-adrenergic receptors, causing vasodilation.

The axon reflex occurs when skin receptors are irritated within the axon of one nerve cell, causing an expansion of the lumen of the vessel in this area.

Thus, the nervous regulation is carried out by the sympathetic department, which can have both an expanding and a narrowing effect. The parasympathetic nervous system has a direct expanding effect.

Humoral regulation carried out by substances of local and systemic action.

Local substances include Ca ions, which have a narrowing effect and are involved in the occurrence of an action potential, calcium bridges, in the process of muscle contraction. K ions also cause vasodilation and in large quantities lead to hyperpolarization of the cell membrane. Na ions in excess can cause an increase blood pressure and water retention in the body, changing the level of hormone secretion.

Hormones have the following effect:

1) vasopressin increases the tone of smooth muscle cells of arteries and arterioles, leading to their narrowing;

2) adrenaline is able to have an expanding and narrowing effect;

3) aldosterone retains Na in the body, affecting the vessels, increasing the sensitivity of the vascular wall to the action of angiotensin;

4) thyroxine stimulates metabolic processes in smooth muscle cells, which leads to narrowing;

5) renin is produced by cells of the juxtaglomerular apparatus and enters the bloodstream, acting on the angiotensinogen protein, which is converted to angiotensin II, leading to vasoconstriction;

6) atriopeptides have an expanding effect.

Metabolites (eg, carbon dioxide, pyruvic acid, lactic acid, H ions) act as cardiac chemoreceptors. vascular system, increasing the speed of transmission of impulses in the central nervous system, which leads to reflex constriction.

Substances of local action produce a variety of effects:

1) mediators of the sympathetic nervous system have mainly a narrowing effect, and parasympathetic - expanding;

2) biologically active substances: histamine - expanding action, and serotonin - narrowing;

3) kinins (bradykinin and kalidin) cause an expanding effect;

4) prostaglandins mainly expand the lumen;

5) endothelial relaxation enzymes (a group of substances formed by endotheliocytes) have a pronounced local narrowing effect.

Thus, vascular tone is influenced by local, nervous and humoral mechanisms.

Under regulation of the heart understand its adaptation to the body's needs for oxygen and nutrients implemented through a change in blood flow.

Since it is derived from the frequency and strength of the contractions of the heart, the regulation can be carried out through a change in the frequency and (or) strength of its contractions.

The mechanisms of its regulation have a particularly powerful effect on the work of the heart during physical activity, when the heart rate and stroke volume can increase by 3 times, the IOC - by 4-5 times, and for high-class athletes - by 6 times. Simultaneously with a change in the performance of the heart with a change in physical activity, emotional and psychological state human metabolism and coronary blood flow change. All this is due to the functioning complex mechanisms regulation of cardiac activity. Among them, intracardiac (intracardiac) and extracardiac (extracardiac) mechanisms are distinguished.

Intracardiac mechanisms of regulation of the heart

Intracardiac mechanisms that ensure self-regulation of cardiac activity are divided into myogenic (intracellular) and nervous (carried out by the intracardiac nervous system).

Intracellular mechanisms are realized due to the properties of myocardial fibers and appear even on an isolated and denervated heart. One of these mechanisms is reflected in the Frank-Starling law, which is also called the law of heterometric self-regulation or the law of the heart.

Frank-Starling Law states that with an increase in myocardial stretch during diastole, the force of its contraction in systole increases. This pattern is revealed when the myocardial fibers are stretched by no more than 45% of their original length. Further stretching of the myocardial fibers leads to a decrease in the efficiency of contraction. Strong stretching creates the risk of developing severe pathology of the heart.

AT vivo the degree of stretching of the ventricles depends on the value of the end-diastolic volume, determined by the filling of the ventricles with blood coming from the veins during diastole, the value of the end-systolic volume, and the force of atrial contraction. The greater the venous return of blood to the heart and the value of the end-diastolic volume of the ventricles, the greater the force of their contraction.

An increase in blood flow to the ventricles is called volume load or preload. An increase in contractile activity of the heart and an increase in volume cardiac output with an increase in preload, they do not require a large increase in energy costs.

One of the patterns of self-regulation of the heart was discovered by Anrep (Anrep phenomenon). It is expressed in the fact that with an increase in resistance to the ejection of blood from the ventricles, the force of their contraction increases. This increase in resistance to the expulsion of blood is called pressure loads or afterload. It increases with an increase in blood. Under these conditions, work increases sharply and energy needs ventricles. An increase in resistance to the expulsion of blood by the left ventricle can also develop with stenosis aortic valve and narrowing of the aorta.

Bowditch phenomenon

Another pattern of self-regulation of the heart is reflected in the Bowditch phenomenon, also called the ladder phenomenon or the law of homeometric self-regulation.

Bowditch's ladder (rhythmoionotropic dependence 1878) — gradual increase the strength of heart contractions to the maximum amplitude, observed when sequentially applying stimuli of constant strength to it.

The law of homeometric self-regulation (the Bowditch phenomenon) is manifested in the fact that with an increase in the heart rate, the force of contractions increases. One of the mechanisms for enhancing myocardial contraction is an increase in the content of Ca 2+ ions in the sarcoplasm of myocardial fibers. At frequent excitations Ca 2+ ions do not have time to be removed from the sarcoplasm, which creates conditions for a more intense interaction between actin and myosin filaments. The Bowditch phenomenon has been identified on an isolated heart.

Under natural conditions, the manifestation of homeometric self-regulation can be observed when sharp rise tone of the sympathetic nervous system and an increase in the level of adrenaline in the blood. AT clinical setting some manifestations of this phenomenon can be observed in patients with tachycardia, when the heart rate increases rapidly.

Neurogenic intracardiac mechanism provides self-regulation of the heart due to reflexes, the arc of which closes within the heart. The bodies of the neurons that make up this reflex arc are located in the intracardiac nerve plexuses and ganglia. Intracardiac reflexes are triggered by stretch receptors present in the myocardium and coronary vessels. G.I. Kositsky in an animal experiment found that when the right atrium is stretched, the contraction of the left ventricle is reflexively increased. Such an effect from the atria to the ventricles is detected only at low blood pressure in the aorta. If the pressure in the aorta is high, then the activation of atrial stretch receptors reflexively inhibits the force of ventricular contraction.

Extracardiac mechanisms of regulation of the heart

Extracardiac mechanisms of regulation of cardiac activity are divided into nervous and humoral. These regulatory mechanisms occur with the participation of structures located outside the heart (CNS, extracardiac autonomic ganglia, endocrine glands).

Intracardiac mechanisms of regulation of the heart

Intracardiac (intracardiac) mechanisms of regulation - regulatory processes that originate inside the heart and continue to function in an isolated heart.

Intracardiac mechanisms are divided into: intracellular and myogenic mechanisms. An example intracellular mechanism regulation is hypertrophy of myocardial cells due to increased synthesis of contractile proteins in sports animals or animals involved in heavy physical work.

Myogenic mechanisms regulation of the activity of the heart include heterometric and homeometric types of regulation. An example heterometric regulation the Frank-Starling law can serve, which states that the greater the blood flow to the right atrium and, accordingly, the increase in the length of the muscle fibers of the heart during diastole, the stronger the heart contracts during systole. homeometric type regulation depends on the pressure in the aorta - the greater the pressure in the aorta, the stronger the heart contracts. In other words, strength heart contraction increases with increasing resistance in the main vessels. In this case, the length of the heart muscle does not change and therefore this mechanism is called homeometric.

Self-regulation of the heart- the ability of cardiomyocytes to independently change the nature of the contraction when the degree of stretching and deformation of the membrane changes. This type of regulation is represented by heterometric and homeometric mechanisms.

Heterometric mechanism - an increase in the force of contraction of cardiomyocytes with an increase in their initial length. It is mediated by intracellular interactions and is associated with a change in the relative position of actin and myosin myofilaments in the myofibrils of cardiomyocytes when the myocardium is stretched by blood entering the heart cavity (an increase in the number of myosin bridges that can connect myosin and actin filaments during contraction). This type of regulation has been cardiopulmonary drug and formulated in the form of the Frank-Starling law (1912).

homeometric mechanism- an increase in the strength of heart contractions with an increase in resistance in the main vessels. The mechanism is determined by the state of cardiomyocytes and intercellular relationships and does not depend on myocardial stretching by the inflowing blood. With homeometric regulation, the efficiency of energy exchange in cardiomyocytes increases and the work of intercalary discs is activated. This type regulation was first discovered by G.V. Anrep in 1912 and is referred to as the Anrep effect.

Cardiocardial reflexes- reflex reactions that occur in the mechanoreceptors of the heart in response to stretching of its cavities. When stretching the atria heartbeat can either speed up or slow down. When stretching the ventricles, as a rule, there is a decrease in heart rate. It has been proven that these reactions are carried out with the help of intracardiac peripheral reflexes (G.I. Kositsky).

Extracardiac mechanisms of regulation of the heart

Extracardiac (extracardiac) mechanisms of regulation - regulatory influences that arise outside the heart and do not function in it in isolation. Extracardiac mechanisms include neuro-reflex and humoral regulation of the activity of the heart.

Nervous regulation The work of the heart is carried out by the sympathetic and parasympathetic divisions of the autonomic nervous system. The sympathetic division stimulates the activity of the heart, and the parasympathetic depresses.

Sympathetic innervation originates in the lateral horns of the upper thoracic segments with the back of the brain, where the bodies of preganglionic sympathetic neurons are located. Having reached the heart, the fibers of the sympathetic nerves penetrate into the myocardium. Excitatory impulses arriving through postganglionic sympathetic fibers cause release in cells contractile myocardium and cells of the conducting system of the norepinephrine mediator. Activation of the sympathetic system and the release of norepinephrine at the same time has certain effects on the heart:

chronotropic effect - an increase in the frequency and strength of heart contractions;
inotropic effect - an increase in the strength of contractions of the myocardium of the ventricles and atria;
dromotropic effect - acceleration of the conduction of excitation in the atrioventricular (atrioventricular) node;
bathmotropic effect - shortening the refractory period of the ventricular myocardium and increasing their excitability.

Parasympathetic innervation heart is carried out by the vagus nerve. The bodies of the first neurons, the axons of which form the vagus nerves, are located in the medulla oblongata. The axons that form the preganglionic fibers penetrate into the cardiac intramural ganglia, where the second neurons are located, the axons of which form the postganglionic fibers that innervate the sinoatrial (sinoatrial) node, the atrioventricular node and the conduction system of the ventricles. Nerve endings parasympathetic fibers release the neurotransmitter acetylcholine. Activation parasympathetic system has a negative chrono-, ino-, dromo-, bathmotropic effects on cardiac activity.

Reflex regulation the work of the heart also occurs with the participation of the autonomic nervous system. Reflex reactions can inhibit and excite cardiac contractions. These changes in the work of the heart occur when various receptors are irritated. For example, in the right atrium and in the mouths of the vena cava there are mechanoreceptors, the excitation of which causes a reflex increase in heart rate. In some parts of the vascular system, there are receptors that are activated when blood pressure changes in the vessels - vascular reflexogenic zones that provide aortic and carotid sinus reflexes. The reflex effect from the mechanoreceptors of the carotid sinus and aortic arch is especially important when blood pressure rises. In this case, the excitation of these receptors occurs and the tone of the vagus nerve increases, as a result of which inhibition of cardiac activity occurs and pressure in large vessels decreases.

Humoral regulation - a change in the activity of the heart under the influence of various, including physiologically active, substances circulating in the blood.

Humoral regulation of the work of the heart is carried out with the help of various compounds. So, an excess of potassium ions in the blood leads to a decrease in the strength of heart contractions and a decrease in the excitability of the heart muscle. An excess of calcium ions, on the contrary, increases the strength and frequency of heart contractions, increases the rate of propagation of excitation through the conduction system of the heart. Adrenaline increases the frequency and strength of heart contractions, and also improves coronary blood flow as a result of stimulation of myocardial p-adrenergic receptors. The hormone thyroxine, corticosteroids, and serotonin have a similar stimulating effect on the heart. Acetylcholine reduces the excitability of the heart muscle and the strength of its contractions, and norepinephrine stimulates cardiac activity.

A lack of oxygen in the blood and an excess of carbon dioxide depress contractile activity myocardium.

The human heart, continuously working, even with a calm lifestyle, pumps into the arterial system about 10 tons of blood per day, 4000 tons per year and about 300,000 tons in a lifetime. At the same time, the heart always accurately responds to the needs of the body, constantly maintaining the necessary level of blood flow.

Adaptation of the activity of the heart to the changing needs of the body occurs with the help of a number of regulatory mechanisms. Some of them are located in the very heart - this is intracardiac regulatory mechanisms. These include intracellular mechanisms of regulation, regulation of intercellular interactions and nervous mechanisms - intracardiac reflexes. To extracardiac regulatory mechanisms include extracardiac nervous and humoral mechanisms of regulation of cardiac activity.

Intracardiac regulatory mechanisms

Intracellular mechanisms of regulation provide a change in the intensity of myocardial activity in accordance with the amount of blood flowing to the heart. This mechanism is called the “law of the heart” (Frank-Sterling law): the force of contraction of the heart (myocardium) is proportional to the degree of its stretching in diastole, i.e. the initial length of its muscle fibers. A stronger myocardial stretch at the time of diastole corresponds to increased blood flow to the heart. At the same time, inside each myofibril, actin filaments are more advanced from the gaps between myosin filaments, which means that the number of reserve bridges increases, i.e. those actin points that connect the actin and myosin filaments at the time of contraction. Therefore, the more each cell is stretched, the more it will be able to shorten during systole. For this reason, the heart pumps into the arterial system the amount of blood that flows to it from the veins.

Regulation of intercellular interactions. It has been established that intercalated discs connecting myocardial cells have a different structure. Some sections of the intercalated discs perform a purely mechanical function, others provide transport through the membrane of the cardiomyocyte of the substances it needs, and others - nexus, or close contacts, conduct excitation from cell to cell. Violation of intercellular interactions leads to asynchronous excitation of myocardial cells and the appearance of cardiac arrhythmia.

Intracardiac peripheral reflexes. So-called peripheral reflexes were found in the heart, the arc of which is closed not in the central nervous system, but in the intramural ganglia of the myocardium. This system includes afferent neurons, whose dendrites form stretch receptors on myocardial fibers and coronary vessels, intercalary and efferent neurons. The axons of the latter innervate the myocardium and smooth muscles of the coronary vessels. These neurons are interconnected by synoptic connections, forming intracardiac reflex arcs.

The experiment showed that an increase in right atrial myocardial stretch (under natural conditions, it occurs with an increase in blood flow to the heart) leads to an increase in left ventricular contractions. Thus, contractions are intensified not only in that part of the heart, the myocardium of which is directly stretched by the inflowing blood, but also in other departments in order to “make room” for the incoming blood and accelerate its release into the arterial system. It has been proven that these reactions are carried out with the help of intracardiac peripheral reflexes.

Similar reactions are observed only against the background of low initial blood filling of the heart and with a small amount of blood pressure in the aortic orifice and coronary vessels. If the chambers of the heart are filled with blood and the pressure in the mouth of the aorta and coronary vessels is high, then the stretching of the venous receivers in the heart inhibits the contractile activity of the myocardium. In this case, the heart ejects into the aorta at the time of systole less than normal, the amount of blood contained in the ventricles. The retention of even a small additional volume of blood in the chambers of the heart increases diastolic pressure in its cavities, which causes a decrease in inflow venous blood to the heart. An excess volume of blood, which, if suddenly released into the arteries, could cause detrimental consequences, is retained in venous system. Such reactions play an important role in the regulation of blood circulation, ensuring the stability of blood supply. arterial system.

A decrease in cardiac output would also pose a danger to the body - it could cause a critical drop in blood pressure. Such a danger is also prevented by regulatory reactions of the intracardiac system.

Insufficient filling of the chambers of the heart and the coronary bed with blood causes an increase in myocardial contractions through intracardiac reflexes. At the same time, at the time of systole, a greater than normal amount of blood contained in them is ejected into the aorta. This prevents the danger of insufficient filling of the arterial system with blood. By the time of relaxation, the ventricles contain less than normal amount of blood, which contributes to increased venous blood flow to the heart.

Under natural conditions, the intracardiac nervous system is not autonomous. Scorch the lowest link in a complex hierarchy nervous mechanisms regulating the activity of the heart. A higher link in the hierarchy are the signals coming through the sympathetic and vagus nerves, the extracardiac nervous system of the regulation of the heart.

Extracardiac regulatory mechanisms

The work of the heart is provided by nervous and humoral mechanisms of regulation. Nervous regulation for the heart does not have a triggering action, since it has automatism. The nervous system provides adaptation of the work of the heart at every moment of adaptation of the body to external conditions and changes in its activities.

Efferent innervation of the heart. The work of the heart is regulated by two nerves: the vagus (or vagus), which belongs to the parasympathetic nervous system, and the sympathetic. These nerves are formed by two neurons. The bodies of the first neurons, the processes of which make up the vagus nerve, are located in the medulla oblongata. The processes of these neurons terminate in the ingramural ganglia of the heart. Here are the second neurons, the processes of which go to the conduction system, myocardium and coronary vessels.

The first neurons of the sympathetic nervous system, which regulates the work of the heart, lie in the lateral horns. I-V chest segments spinal cord. The processes of these neurons end in the cervical and upper thoracic sympathetic nodes. In these nodes are the second neurons, the processes of which go to the heart. Most of sympathetic nerve fibers are sent to the heart from the stellate ganglion. The nerves coming from the right sympathetic trunk mainly approach the sinus node and the muscles of the atria, and the nerves of the left side go to the atrioventricular node and the muscles of the ventricles (Fig. 1).

The nervous system causes the following effects:

chronotropic - change in heart rate;
inotropic - change in the strength of contractions;
bathmotropic - change in the excitability of the heart;
dromotropic - change in myocardial conduction;
tonotropic - change in the tone of the heart muscle.

Nervous extracardiac regulation. Influence of the vagus and sympathetic nerves on the heart

In 1845, the Weber brothers observed cardiac arrest during stimulation of the medulla oblongata in the region of the nucleus of the vagus nerve. After transection of the vagus nerves, this effect was absent. From this it was concluded that the vagus nerve inhibits the activity of the heart. Further research by many scientists expanded the ideas about the inhibitory effect of the vagus nerve. It was shown that when it is irritated, the frequency and strength of heart contractions, excitability and conductivity of the heart muscle decrease. After transection of the vagus nerves, due to the removal of their inhibitory effect, an increase in the amplitude and frequency of heart contractions was observed.

Rice. 1. Scheme of the innervation of the heart:

C - heart; M - medulla; CI - the nucleus that inhibits the activity of the heart; SA - the nucleus that stimulates the activity of the heart; LH - lateral horn of the spinal cord; 75 - sympathetic trunk; V- efferent fibers of the vagus nerve; D - nerve depressor (afferent fibers); S - sympathetic fibers; A - spinal afferent fibers; CS, carotid sinus; B - afferent fibers from the right atrium and vena cava

The influence of the vagus nerve depends on the intensity of stimulation. With weak stimulation, negative chronotropic, inotropic, bathmotropic, dromotropic and tonotropic effects are observed. With strong irritation, cardiac arrest occurs.

The first detailed studies of the sympathetic nervous system on the activity of the heart belong to the Zion brothers (1867), and then I.P. Pavlov (1887).

The Zion brothers observed an increase in heart rate when the spinal cord was stimulated in the region of the location of neurons that regulate the activity of the heart. After transection of the sympathetic nerves, the same irritation of the spinal cord did not cause changes in the activity of the heart. It was found that the sympathetic nerves innervating the heart have a positive effect on all aspects of the activity of the heart. They cause positive chronotropic, inotropic, butmotropic, dromotropic and tonotropic effects.

Further research by I.P. Pavlov, it was shown that the nerve fibers that make up the sympathetic and vagus nerves affect different aspects of the activity of the heart: some change the frequency, while others change the strength of heart contractions. The branches of the sympathetic nerve, when irritated, the strength of the heart contractions increases, were named Pavlov's amplifying nerve. The reinforcing effect of the sympathetic nerves has been found to be associated with an increase in metabolic rate.

As part of the vagus nerve, fibers were also found that affect only the frequency and only the strength of heart contractions.

The frequency and strength of contractions are influenced by the fibers of the vagus and sympathetic nerves, suitable for the sinus node, and the strength of contractions changes under the influence of fibers suitable for the atrioventricular node and the ventricular myocardium.

The vagus nerve easily adapts to irritation, so its effect may disappear despite continued irritation. This phenomenon has been named "escape of the heart from the influence of the vagus." The vagus nerve has a higher excitability, as a result of which it reacts to a lower stimulus than the sympathetic, and a short latent period.

Therefore, when same conditions irritation effect of the vagus nerve appears earlier than the sympathetic.

The mechanism of influence of the vagus and sympathetic nerves on the heart

In 1921, studies by O. Levy showed that the influence of the vagus nerve on the heart is transmitted by the humoral route. In the experiments, Levi applied strong irritation to the vagus nerve, which led to cardiac arrest. Then blood was taken from the heart and acted upon the heart of another animal; at the same time, the same effect arose - inhibition of the activity of the heart. In the same way, the effect of the sympathetic nerve on the heart of another animal can be transferred. These experiments indicate that when the nerves are stimulated, their endings actively secrete active substances, which either inhibit or stimulate the activity of the heart: acetylcholine is released at the vagus nerve endings, and norepinephrine is released at the sympathetic endings.

When the cardiac nerves are irritated, the membrane potential of the muscle fibers of the heart muscle changes under the influence of the mediator. When the vagus nerve is irritated, the membrane hyperpolarizes, i.e. membrane potential increases. The basis of hyperpolarization of the heart muscle is an increase in the permeability of the membrane for potassium ions.

The influence of the sympathetic nerve is transmitted by the neurotransmitter norepinephrine, which causes depolarization of the postsynaptic membrane. Depolarization is associated with an increase in membrane permeability to sodium.

Knowing that the vagus nerve hyperpolarizes and the sympathetic nerve depolarizes the membrane, one can explain all the effects of these nerves on the heart. Since the membrane potential increases when the vagus nerve is irritated, it is required great power irritation to achieve a critical level of depolarization and obtain a response, and this indicates a decrease in excitability (negative bathmotropic effect).

The negative chronotropic effect is due to the fact that when great strength irritation of the vagus hyperpolarization of the membrane is so great that the resulting spontaneous depolarization cannot reach a critical level and the answer does not occur - cardiac arrest occurs.

With a low frequency or strength of stimulation of the vagus nerve, the degree of hyperpolarization of the membrane is less and spontaneous depolarization gradually reaches a critical level, as a result of which rare contractions of the heart occur (negative dromotropic effect).

When the sympathetic nerve is irritated, even with a small force, depolarization of the membrane occurs, which is characterized by a decrease in the magnitude of the membrane and threshold potentials, which indicates an increase in excitability (positive bathmotropic effect).

Since under the influence of the sympathetic nerve the membrane of the muscle fibers of the heart depolarizes, the time of spontaneous depolarization required to reach a critical level and generate an action potential decreases, which leads to an increase in heart rate.

Tone of the centers of the cardiac nerves

The CNS neurons that regulate the activity of the heart are in good shape, i.e. some degree of activity. Therefore, impulses from them constantly come to the heart. The tone of the center of the vagus nerves is especially pronounced. The tone of the sympathetic nerves is weakly expressed, and sometimes absent.

The presence of tonic influences coming from the centers can be observed experimentally. If both vagus nerves are cut, then a significant increase in heart rate occurs. In humans, the influence of the vagus nerve can be turned off by the action of atropine, after which an increase in heart rate is also observed. About availability constant tone centers of the vagus nerves are also evidenced by experiments with the registration of nerve potentials at the moment of irritation. Consequently, the vagus nerves from the central nervous system receive impulses that inhibit the activity of the heart.

After transection of the sympathetic nerves, a slight decrease in the number of heart contractions is observed, which indicates a constantly stimulating effect on the heart of the centers of the sympathetic nerves.

The tone of the centers of the cardiac nerves is maintained by various reflex and humoral influences. Of particular importance are the impulses coming from vascular reflex zones located in the region of the aortic arch and carotid sinus (the place where the carotid artery branches into external and internal). After transection of the depressor nerve and Hering's nerve, coming from these zones to the central nervous system, the tone of the centers of the vagus nerves decreases, resulting in an increase in heart rate.

The state of the heart centers is affected by impulses coming from any other intero- and exteroreceptors of the skin and some internal organs(for example, intestines, etc.).

A number of humoral factors affecting the tone of the cardiac centers have been found. For example, the adrenal hormone adrenaline increases the tone of the sympathetic nerve, and calcium ions have the same effect.

The overlying departments, including the cerebral cortex, also affect the state of the tone of the heart centers.

Reflex regulation of heart activity

Under natural conditions of the body's activity, the frequency and strength of heart contractions constantly change depending on the influence of environmental factors: physical activity, body movement in space, temperature effects, changes in the state of internal organs, etc.

The basis of adaptive changes in cardiac activity in response to various external influences constitute reflex mechanisms. The excitation that has arisen in the receptors, along the afferent pathways, comes to various departments CNS, affects the regulatory mechanisms of cardiac activity. It has been established that the neurons that regulate the activity of the heart are located not only in the medulla oblongata, but also in the cerebral cortex, diencephalon(hypothalamus) and cerebellum. From them, impulses go to the medulla oblongata and spinal cord and change the state of the centers of parasympathetic and sympathetic regulation. From here, the impulses come along the vagus and sympathetic nerves to the heart and cause a slowdown and weakening or an increase and increase in its activity. Therefore, they talk about vagal (inhibitory) and sympathetic (stimulating) reflex influences on the heart.

Constant adjustments to the work of the heart are made by the influence of vascular reflexogenic zones - the aortic arch and carotid sinus (Fig. 2). With an increase in blood pressure in the aorta or carotid arteries, baroreceptors are irritated. The excitation that arises in them passes to the central nervous system and increases the excitability of the center of the vagus nerves, as a result of which the number of inhibitory impulses passing through them increases, which leads to a slowdown and weakening of heart contractions; consequently, the amount of blood ejected by the heart into the vessels decreases, and the pressure decreases.

Rice. 2. Sinocarotid and aortic reflexogenic zones: 1 - aorta; 2 - common carotid arteries; 3 - carotid sinus; 4 - sinus nerve (Goering); 5 - aortic nerve; 6 - carotid body; 7 - vagus nerve; eight - glossopharyngeal nerve; 9 - internal carotid artery

Vagus reflexes include Ashner's eye-heart reflex, Goltz reflex, etc. Reflex Litera It is expressed in a reflex decrease in the number of heart contractions (by 10-20 per minute) that occurs when pressure is applied to the eyeballs. Char reflex lies in the fact that when mechanical irritation is applied to the intestines of a frog (squeezing with tweezers, tapping), the heart stops or slows down. Cardiac arrest can also be observed in a person with a blow in the area solar plexus or when immersed in cold water (vagal reflex from skin receptors).

Sympathetic cardiac reflexes occur with various emotional influences, pain stimuli and physical activity. In this case, an increase in cardiac activity can occur due not only to an increase in the influence of sympathetic nerves, but also to a decrease in the tone of the centers of the vagus nerves. The causative agent of chemoreceptors of vascular reflexogenic zones may be an increased content in the blood various acids (carbon dioxide, lactic acid, etc.) and fluctuations in the active reaction of the blood. At the same time, a reflex increase in the activity of the heart occurs, providing fastest removal these substances from the body and recovery normal composition blood.

Humoral regulation of the activity of the heart

Chemicals that affect the activity of the heart are conventionally divided into two groups: parasympathicotropic (or vagotropic), acting like a vagus, and sympathicotropic - like sympathetic nerves.

To parasympathicotropic substances include acetylcholine and potassium ions. With an increase in their content in the blood, inhibition of the activity of the heart occurs.

To sympathicotropic substances include epinephrine, norepinephrine, and calcium ions. With an increase in their content in the blood, there is an increase and an increase in heart rate. Glucagon, angiotensin and serotonin have a positive inotropic effect, thyroxine has a positive chronotropic effect. Hypoxemia, hyperkainia and acidosis inhibit the contractile activity of the myocardium.

The work of the heart plays a subordinate role, since shifts in metabolism are caused by the nervous system. Content shifts various substances in the blood, in turn, affect the reflex regulation of the cardiovascular system.

The work of the heart is affected by changes in the content of potassium and calcium in the blood. An increase in potassium content has a negative chronotropic, negative inotropic, negative dromotropic, negative bathmotropic and negative tonotropic effects. An increase in calcium has the opposite effect.

For normal operation the heart needs a known ratio of both ions, which act in a similar way to the vagus (potassium) and sympathetic (calcium) nerves.

It is assumed that during the depolarization of the membranes of the muscle fibers of the heart, potassium and ions quickly leave them, which contributes to their contraction. Therefore, the reaction of the blood is important for the contraction of the muscle fibers of the heart.

When the vagus nerves are stimulated, acetylcholine enters the blood, and when the sympathetic nerves are stimulated, a substance similar in composition to adrenaline (O. Levy, 1912, 1921) is norepinephrine. The main mediator of the sympathetic nerves of the mammalian heart is norepinephrine (Euler, 1956). The content of adrenaline in the heart is about 4 times less. The heart more than other organs accumulates adrenaline introduced into the body (40 times more than skeletal muscle).

Acetylcholine is rapidly destroyed. Therefore, it acts only locally, where it is secreted, that is, in the endings of the vagus nerves in the heart. Small doses of acetylcholine excite the automatism of the heart, and large doses inhibit the frequency and strength of heart contractions. Norepinephrine is also destroyed in the blood, but it is more stable than acetylcholine.

When the common trunk of the vagus and sympathetic nerves of the heart is irritated, both substances are formed, but first the action of acetylcholine is manifested, and then norepinephrine.

The introduction of adrenaline and norepinephrine into the body increases the release of acetylcholine, and, conversely, the introduction of acetylcholine increases the formation of adrenaline and norepinephrine. Norepinephrine increases systolic and diastolic blood pressure, while adrenaline only increases systolic.

in the kidneys in normal conditions and especially when their blood supply is reduced, rhenium is formed, which acts on hypertensinogen and converts it into hypertensin, causing vasoconstriction and an increase in blood pressure.

Local vasodilation is caused by the accumulation of acidic metabolic products, especially carbon dioxide, lactic and adenylic acids.

big role in expanding blood vessels acetylcholine and histamine also play. Acetylcholine and its derivatives irritate the endings of parasympathetic nerves and cause local expansion of small arteries. Histamine, a product of protein breakdown, is formed in the wall of the stomach and intestines, in muscles and other organs. Histamine, when it enters, causes capillary dilation. Under normal physiological conditions, histamine in small doses improves the blood supply to organs. In muscles during work, histamine expands the capillaries along with carbon dioxide, lactic and adenylic acids and other substances that are formed during contraction. Histamine also causes the expansion of skin capillaries when exposed to sunlight (ultraviolet part of the spectrum), when the skin is exposed to hydrogen sulfide, heat, when it is rubbed.

An increase in the amount of histamine entering the blood leads to a general expansion of capillaries and a sharp drop in blood pressure - circulatory shock.

The heart is under constant action nervous system and humoral factors. The body is in different conditions existence. The result of the work of the heart is the injection of blood into the systemic and pulmonary circulation.

Assessed by the minute volume of blood. AT normal condition in 1 minute - 5 liters of blood push out both ventricles. In this way we can appreciate the work of the heart.

Systolic blood volume and heart rate - minute volume of blood.

For comparison with different people- introduced cardiac index- how much blood per minute falls on 1 square meter of the body.

In order to change the value of the volume - you need to change these indicators, this happens due to the mechanisms of regulation of the heart.

Minute blood volume (MOV)=5l/min

Cardiac index \u003d IOC / Sm2 \u003d 2.8-3.6 l / min / m2

IVO=systolic volume*rate/min

Mechanisms of regulation of the heart

Intracardiac (intracardiac)
Extracardiac (Extracardiac)

To intracardiac mechanisms include the presence of tight contacts between the cells of the working myocardium, the conduction system of the heart coordinates the individual work of the chambers, intracardiac nerve elements, hydrodynamic interaction between individual chambers.

Extracardiac - nervous and humoral mechanism , which change the work of the heart and adapt the work of the heart to the needs of the body.

Nervous regulation of the heart is carried out by the autonomic nervous system. The heart receives innervation from parasympathetic(wandering) and sympathetic(lateral horns of the spinal cord T1-T5) nerves.

Ganglia of the parasympathetic system lie inside the heart and there the preganglionic fibers switch to postganglionic. Preganglionic nuclei - medulla oblongata.

Sympathetic- are interrupted in the stellate ganglion, where the postganglionic cells that go to the heart will already be located.

Right vagus nerve- innervates the sino-atrial node, the right atrium,

Left vagus nerve to the atrioventricular node and right atrium

Right sympathetic nerve- to the sinus node, right atrium and ventricle

Left sympathetic nerve- to the atrioventricular nodes and to the left half of the heart.

In the ganglia, acetylcholine acts on N-cholinergic receptors

Sympathetic secrete norepinephrine, which acts on adrenergic receptors (B1)

Parasympathetic- acetylcholine at M-cholino receptors (muscarino)

Influence on the work of the heart.

Chronotropic effect (on heart rate)
Inotropic (on the strength of heart contractions)
Bathmotropic effect (on excitability)
Dromotropic (for conductivity)

1845 - Weber brothers - discovered the influence of the vagus nerve. They cut a nerve in his neck. When the right vagus nerve was irritated, the frequency of contractions decreased, but it could stop - negative chronotropic effect(suppression of automatic sinus node). If the left vagus nerve was irritated, conduction worsened. The atrioventricular nerve is responsible for delaying excitation.

vagus nerves reduce myocardial excitability and reduce the frequency of contractions.

Under the action of the vagus nerve - slowing down the diastolic depolarization of p - cells, pacemakers. Increases the release of potassium. Although the vagus nerve causes cardiac arrest, it cannot be done completely. There is a resumption of contraction of the heart - escape from the influence of the vagus nerve and the resumption of the work of the heart is due to the fact that the automation from the sinus node passes to the atrioventricular node, which returns the work of the heart with a frequency of 2 times less.

Sympathetic Influences- studied by the Zion brothers - 1867. When stimulated by sympathetic nerves, Ziones found that sympathetic nerves give positive chronotropic effect. Pavlov studied further. In 1887 he published his work on the influence of nerves on the functioning of the heart. In his research, he discovered that individual branches, without changing the frequency, increase the strength of contractions - positive inotropic effect. Further, the bamotropic and dromotropic effects were discovered.

Positive Influences for the work of the heart is due to the influence of norepinephrine on beta 1 adrenoreceptors, which activate adenylate cyclase, promote the formation of cyclic AMP, and increase the ion permeability of the membrane. Diastolic depolarization occurs at a faster rate and this causes a more frequent rhythm. Sympathetic nerves increase the breakdown of glycogen, ATP, thereby providing the myocardium with energetic resources increases the excitability of the heart. The minimum duration of the action potential in the sinus node is set to 120 ms, i.e. theoretically, the heart could give us the number of contractions - 400 per minute, but the atrioventricular node is not able to conduct more than 220. The ventricles are maximally reduced with a frequency of 200-220. The role of mediators in the transmission of excitation to the hearts was established by Otto Levi in 1921. He used 2 isolated frog hearts, and these hearts were fed from the 1st cannula. In one heart, nerve conductors were preserved. When one heart was irritated, he observed what was happening in the other. When the vagus nerve was irritated, acetylcholine was released - through the liquid it influenced the work of another heart.

The release of norepinephrine increases the work of the heart. The discovery of this neurotransmitter excitation brought Levy the Nobel Prize.

The nerves of the heart are in a state of constant excitement - tone. At rest, the tone of the vagus nerve is especially pronounced. When transection of the vagus nerve, there is an increase in the work of the heart by 2 times. The vagus nerves constantly depress the automation of the sinus node. Normal frequency- 60-100 cuts. Switching off the vagus nerves (transection, cholinergic receptor blockers (atropine)) cause an increase in the work of the heart. The tone of the vagus nerves is determined by the tone of its nuclei. Excitation of the nuclei is maintained reflexively due to impulses that come from the baroreceptors of blood vessels to the medulla oblongata from the aortic arch and carotid sinus. Breathing also affects the tone of the vagus nerves. In connection with breathing - respiratory arrhythmia, when on exhalation there is an increase in the work of the heart.

The tone of the sympathetic nerves of the heart at rest is weakly expressed. If you cut the sympathetic nerves - the frequency of contractions decreases by 6-10 beats per minute. This tone increases with physical activity, increases with various diseases. The tone is well expressed in children, in newborns (129-140 beats per minute)

The heart is still subject to the action of the humoral factor- hormones (adrenal glands - adrenaline, noradarenaline, thyroid gland - thyroxine and mediator acetylcholine)

Hormones have + influence on all 4 properties of the heart. The electrolyte composition of the plasma affects the heart and the work of the heart changes with changes in the concentration of potassium and calcium. Hyperkalemia - increased content potassium in the blood - very dangerous state, this can lead to cardiac arrest in diastole. hypokalimi I - a less dangerous condition on the cardiogram, a change in the PQ distance, a perversion of the T wave. The heart stops in systole. The body temperature also affects the heart - an increase in body temperature by 1 degree - an increase in the work of the heart - by 8-10 beats per minute.

Systolic volume

Preload (the degree of stretching of cardiomyocytes before their contraction. The degree of stretching will be determined by the volume of blood that will be in the ventricles.)
Contractility (Stretching of cardiomyocytes, where the length of the sarcomere changes. Usually 2 microns thick. The maximum contraction force of cardiomyocytes is up to 2.2 microns. This optimal ratio between the bridges of myosin and actin filaments, when their interaction is maximum. This determines the strength of the contraction further stretching to 2.4 reduces contractility. This adjusts the heart to the flow of blood, with its increase - a greater force of contraction. The force of myocardial contraction can change without changing the amount of blood, due to the hormones of adrenaline and norepinephrine, calcium ions, etc. - the force of myocardial contraction increases)
Afterload (Afterload is the tension in the myocardium that must occur in systole to open the semilunar valves. The magnitude of the afterload is determined by the value systolic pressure in the aorta and pulmonary trunk)

Laplace's law

Stress degree of the ventricular wall = Intragastric pressure * radius / wall thickness. The greater the intraventricular pressure and the larger the radius (the size of the lumen of the ventricle), the greater the tension of the ventricular wall. The increase in thickness - affects inversely proportionally. T=P*r/W

The amount of blood flow depends not only on the minute volume, but it is also determined by the amount of peripheral resistance that occurs in the vessels.

Blood vessels have a powerful effect on blood flow. All blood vessels are lined with endothelium. Next is the elastic frame, and in the muscle cells there are also smooth muscle cells and collagen fibers. The vessel wall obeys Laplace's law. If there is intravascular pressure inside the vessel and the pressure causes tension in the vessel wall, then there is a state of tension in the wall. Also affects the radius of the vessels. The stress will be determined by the product of the pressure and the radius. In the vessels, we can distinguish the basal vascular tone. Vascular tone, which is determined by the degree of contraction.

Basal tone- determined by the degree of stretching

Neurohumoral tone- influence of nervous and humoral factors on vascular tone.

The increased radius puts more stress on the walls of the vessels than in the can, where the radius is smaller. In order to carry out normal blood flow and adequate blood supply was provided, there are mechanisms for regulating blood vessels.

They are represented by 3 groups

Local regulation of blood flow in tissues
Nervous regulation
Humoral regulation

Tissue blood flow provides

Delivery of oxygen to cells

Delivery of nutrients (glucose, amino acids, fatty acid and etc.)

CO2 removal

Removal of H+ protons

Blood flow regulation- short-term (a few seconds or minutes as a result of local changes in tissues) and long-term (occurs over hours, days and even weeks. This regulation is associated with the formation of new vessels in the tissues)

The formation of new vessels is associated with an increase in tissue volume, an increase in the intensity of metabolism in the tissue.

Angiogenesis- the formation of blood vessels. This is under the influence of growth factors - vascular endothelial growth factor. Fibroblast growth factor and angiogenin

Humoral regulation of blood vessels

1. Vasoactive metabolites

a. Vasodilation provides - decrease in pO2, Increase - CO2, t, K + lactic acid, adenosine, histamine

b. vasoconstriction cause - an increase in serotonin and a decrease in temperature.

2. Influence of the endothelium

Endothelins (1,2,3). - constriction

Nitric oxide NO - expansion

Formation of nitric oxide (NO)

Release of Ach, bradykinin
Opening of Ca+ channels in the endothelium
Binding of Ca+ to calmodulin and its activation
Enzyme activation (nitric oxide synthetase)
Conversion of Lfrginine to NO

Mechanism of actionNO

NO - activates guanylcyclase GTP - cGMP - opening of K channels - exit of K + - hyperpolarization - decrease in calcium permeability - expansion of smooth muscles and vasodilation.

It has a cytotoxic effect on bacteria and tumor cells when isolated from leukocytes

It is a mediator of the transmission of excitation in some neurons of the brain

Mediator of parasympathetic postganglionic fibers for penile vessels

Possibly involved in the mechanisms of memory and thinking

A.Bradikinin

B. Kallidin

Kininogen with VMV - bradykinin (with Plasma kallikrein)

Kininogen with YVD - kallidin (with tissue kallikrein)

Kinins are formed when vigorous activity sweat glands, salivary glands and pancreas.

Regulation of the heart

If removed from a corpse recently dead person heart and pass through its vessels a nutrient fluid enriched with oxygen, it can contract for some time outside the body. In this case, the contractions of the atria, ventricles and pause will take place in the normal sequence. This is because there are neuromuscular structures in the heart muscle that can ensure its work.

The ability of an organ to be rhythmically excited without external stimuli under the influence of impulses that arise in itself is called automatism. The heart is also automatic.

Fast and accurate adaptation of blood circulation to the needs of the body is achieved through a variety of mechanisms. regulation of the heart. Regulatory mechanisms can be divided into extracardiac mechanisms(nervous and humoral regulation), and intracardiac mechanisms(self-regulation).

1. Nervous and humoral regulation form a single neuro-humoral mechanism for regulating the work of the heart, providing normal functioning organisms under changing environmental conditions.

Nervous regulation The work of the heart is carried out by the autonomic nervous system. Nerve impulses coming to the heart along the branches of the vagus nerve (parasympathetic nervous system) reduce the strength and frequency of contractions. The impulses that come to the heart along the sympathetic nerves increase the frequency and strength of heart contractions. Their centers are in cervical region spinal cord. sympathetic activity and parasympathetic divisions regulates the central nervous system feedback: with an increase in sympathetic activity, parasympathetic activity decreases and vice versa. The central nervous system constantly controls the work of the heart through nerve impulses. For example, a person's heart beats faster when he quickly gets up from a lying position. The point is that the transition vertical position leads to the accumulation of blood in the lower part of the body and reduces the blood supply to the upper part, especially the brain. To restore blood flow in the upper body, impulses are sent from the vascular receptors to the central nervous system. From there to the heart nerve fibers impulses are transmitted that accelerate the contraction of the heart.

The central nervous system does not change the sequence of atrial and ventricular contractions, but it can change their rhythm. When a person is resting, the heart works more slowly. When he is busy with strenuous physical work, the heart works harder and more often. This happens because two nerves approach the heart: sympathetic- accelerating and wandering slowing down the activity of the heart.

The sympathetic and vagus nerves belong to the autonomic nervous system. They regulate the work of not only the heart, but also blood vessels. So, the sympathetic nerve not only enhances the activity of the heart, but also narrows the arterial vessels extending from the heart. As a result, the pressure on the walls of arterial vessels increases. But if it reaches a critical level, the action of the vagus nerve increases, which not only weakens the activity of the heart, but also expands the lumen of the arterial vessels. This leads to a decrease in pressure. As a result, healthy person blood pressure level is maintained within certain limits. If it becomes below normal, the action of the sympathetic nerves will increase, which will correct the situation.

Humoral regulation(lat. humor- liquid) - one of the mechanisms for coordinating vital processes in the body, carried out through the liquid media of the body (blood, lymph, tissue fluid) with the help of biologically active substances released by cells, tissues and organs during their functioning. Important role hormones play a role in humoral regulation. For example, acetylcholine has a depressing effect on the functioning of the heart, while the sensitivity to this substance is so great that at a dose of 0.0000001 mg it clearly slows down the heart rate. Adrenaline has the opposite effect, which even in very small doses enhances the work of the heart. The heart is sensitive to the ionic composition of the blood. Calcium ions increase the excitability of myocardial cells, but their high saturation can cause cardiac arrest, potassium ions inhibit functional activity hearts.

2. The second level is presented intracardiac mechanisms , regulating the work of the heart at the organ level, as well as intracellular mechanisms that regulate the strength of heart contractions, the speed and degree of myocardial relaxation.

In the heart, the intraorgan nervous system functions, forming miniature reflex arcs. Thus, an increase in blood flow to the right atrium and stretching of its walls lead to an increase in the contraction of the left ventricle.

Intracellular mechanisms of regulation take place, for example, in athletes. Regular muscle load leads to an increase in the synthesis of myocardial contractile proteins and a thickening of the walls of the heart and an increase in its size. So, if the mass of an untrained heart is 300 g, then in athletes it increases to 500 g.

The heart is able to be excited without external stimuli, under the influence of impulses arising in itself. The sequence of contractions of the atria, ventricles and pause is determined by the internal automatism of the heart.

Regulates the work of the heart in general vegetative department nervous system. The sympathetic nerve accelerates and enhances the activity of the heart, the vagus nerve slows it down. These nerves also affect the lumen of the vessels extending from the heart. Thanks to their coordinated work, a stable arterial pressure. The heart and blood vessels are also affected humoral factors, in particular the hormone adrenaline, acetylcholine, calcium and potassium salts, as well as some other substances.