rheological action. Blood is like living tissue. Hyperviscosity Syndrome

Rheology is a field of mechanics that studies the features of the flow and deformation of real continuous media, one of the representatives of which are non-Newtonian fluids with structural viscosity. A typical non-Newtonian fluid is blood. Blood rheology, or hemorheology, studies the mechanical patterns and especially changes in the physical and colloidal properties of blood during circulation at different speeds and in different parts of the vascular bed. The movement of blood in the body is determined by the contractility of the heart, the functional state of the bloodstream, and the properties of the blood itself. At relatively low linear flow velocities, blood particles are displaced parallel to each other and to the axis of the vessel. In this case, the blood flow has a layered character, and such a flow is called laminar.

If the linear velocity increases and exceeds a certain value, which is different for each vessel, then the laminar flow turns into a chaotic, vortex, which is called "turbulent". The speed of blood movement at which laminar flow becomes turbulent is determined using the Reynolds number, which for blood vessels is approximately 1160. Data on Reynolds numbers indicate that turbulence is possible only at the beginning of the aorta and at the branches of large vessels. The movement of blood through most vessels is laminar. In addition to the linear and volumetric blood flow velocity, the movement of blood through the vessel is characterized by two more important parameters, the so-called "shear stress" and "shear rate". Shear stress means the force acting on a unit surface of the vessel in the direction tangential to the surface and is measured in dynes/cm2, or in Pascals. The shear rate is measured in reciprocal seconds (s-1) and means the magnitude of the velocity gradient between parallel moving layers of fluid per unit distance between them.

Blood viscosity is defined as the ratio of shear stress to shear rate, and is measured in mPas. The viscosity of whole blood depends on the shear rate in the range of 0.1 - 120 s-1. At a shear rate >100 s-1, the changes in viscosity are not so pronounced, and after reaching a shear rate of 200 s-1, the blood viscosity practically does not change. The value of viscosity measured at high shear rate (more than 120 - 200 s-1) is called asymptotic viscosity. The principal factors affecting blood viscosity are hematocrit, plasma properties, aggregation and deformability of cellular elements. Considering the vast majority of erythrocytes compared to leukocytes and platelets, the viscous properties of blood are determined mainly by red cells.

The main factor that determines blood viscosity is the volumetric concentration of red blood cells (their content and average volume), called hematocrit. Hematocrit, determined from a blood sample by centrifugation, is approximately 0.4 - 0.5 l / l. Plasma is a Newtonian fluid, its viscosity depends on temperature and is determined by the composition of blood proteins. Most of all, plasma viscosity is affected by fibrinogen (plasma viscosity is 20% higher than serum viscosity) and globulins (especially Y-globulins). According to some researchers, a more important factor leading to a change in plasma viscosity is not the absolute amount of proteins, but their ratios: albumin / globulins, albumin / fibrinogen. The viscosity of blood increases with its aggregation, which determines the non-Newtonian behavior of whole blood, this property is due to the aggregation ability of red blood cells. Physiological aggregation of erythrocytes is a reversible process. In a healthy organism, a dynamic process of "aggregation - disaggregation" continuously occurs, and disaggregation dominates over aggregation.

The property of erythrocytes to form aggregates depends on hemodynamic, plasma, electrostatic, mechanical, and other factors. Currently, there are several theories explaining the mechanism of erythrocyte aggregation. The most famous today is the theory of the bridge mechanism, according to which bridges from fibrinogen or other large molecular proteins, in particular Y-globulins, are adsorbed on the surface of the erythrocyte, which, with a decrease in shear forces, contribute to the aggregation of erythrocytes. The net aggregation force is the difference between the bridge force, the electrostatic repulsion force of the negatively charged red blood cells, and the shear force causing disaggregation. The mechanism of fixation on erythrocytes of negatively charged macromolecules: fibrinogen, Y-globulins is not yet fully understood. There is a point of view that the adhesion of molecules occurs due to weak hydrogen bonds and dispersed van der Waals forces.

There is an explanation for the aggregation of erythrocytes through depletion - the absence of high molecular weight proteins near the erythrocytes, resulting in an "interaction pressure" similar in nature to the osmotic pressure of a macromolecular solution, which leads to the convergence of suspended particles. In addition, there is a theory according to which erythrocyte aggregation is caused by erythrocyte factors themselves, which lead to a decrease in the zeta potential of erythrocytes and a change in their shape and metabolism. Thus, due to the relationship between the aggregation ability of erythrocytes and blood viscosity, a comprehensive analysis of these indicators is necessary to assess the rheological properties of blood. One of the most accessible and widely used methods for measuring erythrocyte aggregation is the assessment of the erythrocyte sedimentation rate. However, in its traditional version, this test is uninformative, since it does not take into account the rheological characteristics of the blood.

Blood rheology(from the Greek word rheos- flow, flow) - blood fluidity, determined by the totality of the functional state of blood cells (mobility, deformability, aggregation activity of erythrocytes, leukocytes and platelets), blood viscosity (concentration of proteins and lipids), blood osmolarity (glucose concentration). The key role in the formation of rheological parameters of blood belongs to blood cells, primarily erythrocytes, which make up 98% of the total volume of blood cells. .

The progression of any disease is accompanied by functional and structural changes in certain blood cells. Of particular interest are changes in erythrocytes, whose membranes are a model of the molecular organization of plasma membranes. Their aggregation activity and deformability, which are the most important components in microcirculation, largely depend on the structural organization of red blood cell membranes. Blood viscosity is one of the integral characteristics of microcirculation that significantly affects hemodynamic parameters. The share of blood viscosity in the mechanisms of regulation of blood pressure and organ perfusion is reflected by the Poiseuille law: MOorgana = (Rart - Rven) / Rlok, where Rlok= 8Lh / pr4, L is the length of the vessel, h is the viscosity of the blood, r is the diameter of the vessel. (Fig.1).

A large number of clinical studies on blood hemorheology in diabetes mellitus (DM) and metabolic syndrome (MS) have revealed a decrease in the parameters characterizing the deformability of erythrocytes. In patients with diabetes, the reduced ability of erythrocytes to deform and their increased viscosity are the result of an increase in the amount of glycated hemoglobin (HbA1c). It has been suggested that the resulting difficulty in blood circulation in the capillaries and the change in pressure in them stimulates the thickening of the basement membrane and leads to a decrease in the coefficient of oxygen delivery to the tissues, i.e. abnormal red blood cells play a triggering role in the development of diabetic angiopathy.

A normal erythrocyte under normal conditions has a biconcave disk shape, due to which its surface area is 20% larger compared to a sphere of the same volume. Normal erythrocytes are able to significantly deform when passing through the capillaries, while not changing their volume and surface area, which maintains the diffusion of gases at a high level throughout the entire microvasculature of various organs. It has been shown that with a high deformability of erythrocytes, the maximum transfer of oxygen to cells occurs, and with a deterioration in deformability (increased rigidity), the supply of oxygen to cells sharply decreases, and tissue pO2 drops.

Deformability is the most important property of erythrocytes, which determines their ability to perform a transport function. This ability of erythrocytes to change their shape at a constant volume and surface area allows them to adapt to the conditions of blood flow in the microcirculation system. The deformability of erythrocytes is due to factors such as intrinsic viscosity (concentration of intracellular hemoglobin), cellular geometry (maintaining the shape of a biconcave disk, volume, surface to volume ratio) and membrane properties that provide the shape and elasticity of erythrocytes.
Deformability largely depends on the degree of compressibility of the lipid bilayer and the constancy of its relationship with the protein structures of the cell membrane.

The elastic and viscous properties of the erythrocyte membrane are determined by the state and interaction of cytoskeleton proteins, integral proteins, the optimal content of ATP, Ca ++, Mg ++ ions and hemoglobin concentration, which determine the internal fluidity of the erythrocyte. The factors that increase the rigidity of erythrocyte membranes include: the formation of stable compounds of hemoglobin with glucose, an increase in the concentration of cholesterol in them and an increase in the concentration of free Ca ++ and ATP in the erythrocyte.

Violation of the deformability of erythrocytes occurs when the lipid spectrum of membranes changes and, first of all, when the ratio of cholesterol / phospholipids is disturbed, as well as in the presence of products of membrane damage as a result of lipid peroxidation (LPO). LPO products have a destabilizing effect on the structural and functional state of erythrocytes and contribute to their modification.
The deformability of erythrocytes decreases due to the absorption of plasma proteins, primarily fibrinogen, on the surface of erythrocyte membranes. This includes changes in the membranes of the erythrocytes themselves, a decrease in the surface charge of the erythrocyte membrane, a change in the shape of the erythrocytes and changes in the plasma (protein concentration, lipid spectrum, total cholesterol, fibrinogen, heparin). Increased aggregation of erythrocytes leads to disruption of transcapillary metabolism, release of biologically active substances, stimulates platelet adhesion and aggregation.

Deterioration of erythrocyte deformability accompanies the activation of lipid peroxidation processes and a decrease in the concentration of antioxidant system components in various stressful situations or diseases, in particular, in diabetes and cardiovascular diseases.
Activation of free radical processes causes disturbances in hemorheological properties, realized through damage to circulating erythrocytes (oxidation of membrane lipids, increased rigidity of the bilipid layer, glycosylation and aggregation of membrane proteins), having an indirect effect on other indicators of the oxygen transport function of the blood and oxygen transport in tissues. Significant and ongoing activation of lipid peroxidation in serum leads to a decrease in the deformability of erythrocytes and an increase in their aregation. Thus, erythrocytes are among the first to respond to LPO activation, first by increasing the deformability of erythrocytes, and then, as LPO products accumulate and antioxidant protection is depleted, to an increase in the rigidity of erythrocyte membranes, their aggregation activity and, accordingly, to changes in blood viscosity.

The oxygen-binding properties of blood play an important role in the physiological mechanisms of maintaining a balance between the processes of free radical oxidation and antioxidant protection in the body. These properties of blood determine the nature and magnitude of oxygen diffusion to tissues, depending on the need for it and the effectiveness of its use, contribute to the pro-oxidant-antioxidant state, showing either antioxidant or pro-oxidant qualities in various situations.

Thus, the deformability of erythrocytes is not only a determining factor in the transport of oxygen to peripheral tissues and ensuring their need for it, but also a mechanism that affects the effectiveness of the antioxidant defense and, ultimately, the entire organization of maintaining the prooxidant-antioxidant balance of the whole organism.

With insulin resistance (IR), an increase in the number of erythrocytes in the peripheral blood was noted. In this case, increased aggregation of erythrocytes occurs due to an increase in the number of adhesion macromolecules and a decrease in the deformability of erythrocytes is noted, despite the fact that insulin at physiological concentrations significantly improves the rheological properties of blood.

At present, the theory that considers membrane disorders as the leading causes of organ manifestations of various diseases, in particular, in the pathogenesis of arterial hypertension in MS, has become widespread.

These changes also occur in various types of blood cells: erythrocytes, platelets, lymphocytes. .

Intracellular redistribution of calcium in platelets and erythrocytes entails damage to microtubules, activation of the contractile system, release of biologically active substances (BAS) from platelets, triggering their adhesion, aggregation, local and systemic vasoconstriction (thromboxane A2).

In patients with hypertension, changes in the elastic properties of erythrocyte membranes are accompanied by a decrease in their surface charge, followed by the formation of erythrocyte aggregates. The maximum rate of spontaneous aggregation with the formation of persistent erythrocyte aggregates was noted in patients with grade III AH with a complicated course of the disease. Spontaneous aggregation of erythrocytes enhances the release of intra-erythrocyte ADP, followed by hemolysis, which causes conjugated platelet aggregation. Hemolysis of erythrocytes in the microcirculation system can also be associated with a violation of the deformability of erythrocytes, as a limiting factor in their life expectancy.

Particularly significant changes in the shape of erythrocytes are observed in the microvasculature, some of the capillaries of which have a diameter of less than 2 microns. Vital microscopy of blood (approx. native blood) shows that erythrocytes moving in the capillary undergo significant deformation, while acquiring various shapes.

In patients with hypertension combined with diabetes, an increase in the number of abnormal forms of erythrocytes was revealed: echinocytes, stomatocytes, spherocytes and old erythrocytes in the vascular bed.

Leukocytes make a great contribution to hemorheology. Due to their low ability to deform, leukocytes can be deposited at the level of the microvasculature and significantly affect the peripheral vascular resistance.

Platelets occupy an important place in the cellular-humoral interaction of hemostasis systems. Literature data indicate a violation of the functional activity of platelets already at an early stage of AH, which is manifested by an increase in their aggregation activity, an increase in sensitivity to aggregation inducers.

The researchers noted a qualitative change in platelets in patients with hypertension under the influence of an increase in free calcium in the blood plasma, which correlates with the magnitude of systolic and diastolic blood pressure. Electron - microscopic examination of platelets in patients with hypertension revealed the presence of various morphological forms of platelets caused by their increased activation. The most characteristic are such changes in shape as the pseudopodial and hyaline type. A high correlation was noted between an increase in the number of platelets with their altered shape and the frequency of thrombotic complications. In MS patients with AH, an increase in platelet aggregates circulating in the blood is detected. .

Dyslipidemia contributes significantly to functional platelet hyperactivity. An increase in the content of total cholesterol, LDL and VLDL in hypercholesterolemia causes a pathological increase in the release of thromboxane A2 with an increase in platelet aggregability. This is due to the presence of apo-B and apo-E lipoprotein receptors on the surface of platelets. On the other hand, HDL reduces the production of thromboxane, inhibiting platelet aggregation, by binding to specific receptors.

Arterial hypertension in MS is determined by a variety of interacting metabolic, neurohumoral, hemodynamic factors and the functional state of blood cells. Normalization of blood pressure levels may be due to total positive changes in biochemical and rheological blood parameters.

The hemodynamic basis of AH in MS is a violation of the relationship between cardiac output and TPVR. First, there are functional changes in blood vessels associated with changes in blood rheology, transmural pressure and vasoconstrictor reactions in response to neurohumoral stimulation, then morphological changes in microcirculation vessels are formed that underlie their remodeling. With an increase in blood pressure, the dilatation reserve of arterioles decreases, therefore, with an increase in blood viscosity, OPSS change to a greater extent than under physiological conditions. If the reserve of dilatation of the vascular bed is exhausted, then the rheological parameters become of particular importance, since the high blood viscosity and the reduced deformability of erythrocytes contribute to the growth of OPSS, preventing the optimal delivery of oxygen to the tissues.

Thus, in MS, as a result of protein glycation, in particular erythrocytes, which is documented by a high content of HbAc1, there are violations of blood rheological parameters: a decrease in elasticity and mobility of erythrocytes, an increase in platelet aggregation activity and blood viscosity, due to hyperglycemia and dyslipidemia. Altered rheological properties of blood contribute to the growth of total peripheral resistance at the level of microcirculation and, in combination with sympathicotonia that occurs with MS, underlie the genesis of AH. Pharmacological (biguanides, fibrates, statins, selective beta-blockers) correction of the glycemic and lipid profiles of the blood, contribute to the normalization of blood pressure. An objective criterion for the effectiveness of ongoing therapy in MS and DM is the dynamics of HbAc1, a decrease in which by 1% is accompanied by a statistically significant decrease in the risk of developing vascular complications (MI, cerebral stroke, etc.) by 20% or more.

Fragment of the article by A.M. Shilov, A.Sh. Avshalumov, E.N. Sinitsina, V.B. Markovsky, Poleshchuk O.I. MMA them. I.M. Sechenov

Blood is a special liquid tissue of the body, in which the shaped elements are freely suspended in a liquid medium. Blood as a tissue has the following features: 1) all its constituent parts are formed outside the vascular bed; 2) the intercellular substance of the tissue is liquid; 3) the main part of the blood is in constant motion. The main functions of blood are transport, protective and regulatory. All three functions of the blood are interconnected and inseparable from each other. The liquid part of the blood - plasma - has a connection with all organs and tissues and reflects the biochemical and biophysical processes occurring in them. The amount of blood in a person under normal conditions is from 1/13 to 1/20 of the total mass (3-5 liters). The color of blood depends on the content of oxyhemoglobin in it: arterial blood is bright red (rich in oxyhemoglobin), and venous blood is dark red (poor in oxyhemoglobin). The viscosity of blood is on average 5 times higher than the viscosity of water. The surface tension is less than the tension of water. In the composition of the blood, 80% is water, 1% is inorganic substances (sodium, chlorine, calcium), 19% is organic substances. Blood plasma contains 90% water, its specific gravity is 1030, lower than that of blood (1056-1060). Blood as a colloidal system has colloidal osmotic pressure, i.e., it is able to retain a certain amount of water. This pressure is determined by the dispersion of proteins, salt concentration and other impurities. Normal colloid osmotic pressure is about 30 mm. water. Art. (2940 Pa). The formed elements of blood are erythrocytes, leukocytes and platelets. On average, 45% of the blood is formed elements, and 55% is plasma. The formed elements of the blood are a heteromorphic system consisting of elements differently differentiated in structural and functional terms. Combine their common histogenesis and coexistence in the peripheral blood.

blood plasma- the liquid part of the blood, in which the formed elements are suspended. The percentage of plasma in the blood is 52-60%. Microscopically, it is a homogeneous, transparent, somewhat yellowish liquid that collects in the upper part of the vessel with blood after sedimentation of formed elements. Histologically, plasma is the intercellular substance of the liquid tissue of the blood.

Blood plasma consists of water, in which substances are dissolved - proteins (7-8% of the plasma mass) and other organic and mineral compounds. The main plasma proteins are albumins - 4-5%, globulins - 3% and fibrinogen - 0.2-0.4%. Nutrients (in particular, glucose and lipids), hormones, vitamins, enzymes, and intermediate and end products of metabolism are also dissolved in the blood plasma. On average, 1 liter of human plasma contains 900-910 g of water, 65-85 g of protein and 20 g of low molecular weight compounds. Plasma density ranges from 1.025 to 1.029, pH - 7.34-7.43.

Rheological properties of blood.

Blood is a suspension of cells and particles suspended in plasma colloids. This is a typically non-Newtonian fluid, the viscosity of which, unlike the Newtonian, varies hundreds of times in different parts of the circulatory system, depending on the change in blood flow velocity. For the viscosity properties of blood, the protein composition of the plasma is important. Thus, albumins reduce the viscosity and ability of cells to aggregate, while globulins act in the opposite way. Fibrinogen is especially active in increasing the viscosity and tendency of cells to aggregate, the level of which changes under any stressful conditions. Hyperlipidemia and hypercholesterolemia also contribute to the violation of the rheological properties of the blood. Hematocrit- one of the important indicators associated with blood viscosity. The higher the hematocrit, the greater the viscosity of the blood and the worse its rheological properties. Hemorrhage, hemodilution and, conversely, plasma loss and dehydration significantly affect the rheological properties of blood. Therefore, for example, controlled hemodilution is an important means of preventing rheological disorders during surgical interventions. With hypothermia, blood viscosity increases 1.5 times compared to that at 37 degrees C, but if the hematocrit is reduced from 40% to 20%, then with such a temperature difference, the viscosity will not change. Hypercapnia increases blood viscosity, so it is less in venous blood than in arterial blood. With a decrease in blood pH by 0.5 (with high hematocrit), blood viscosity increases threefold.

DISORDERS OF BLOOD RHEOLOGICAL PROPERTIES.

The main phenomenon of blood rheological disorders is erythrocyte aggregation, coinciding with an increase in viscosity. The slower the blood flow, the more likely this phenomenon is to develop. The so-called false aggregates ("coin columns") are of a physiological nature and decompose into healthy cells when conditions change. True aggregates that arise in pathology do not disintegrate, giving rise to the phenomenon of sludge (translated from English as "sucks"). Cells in aggregates are covered with a protein film that glues them into irregularly shaped clumps. The main factor causing aggregation and sludge is a violation of hemodynamics - a slowdown in blood flow that occurs in all critical conditions - traumatic shock, hemorrhage, clinical death, cardiogenic shock, etc. Very often, hemodynamic disorders are combined with hyperglobulinemia in such severe conditions as peritonitis, acute intestinal obstruction, acute pancreatitis, prolonged compression syndrome, burns. They increase the aggregation of the state of fat, amniotic and air embolism, damage to erythrocytes during cardiopulmonary bypass, hemolysis, septic shock, etc., that is, all critical conditions. It can be said that the main cause of blood flow disturbance in the capillary is a change in the rheological properties of the blood, which in turn depend mainly on the blood flow velocity. Therefore, blood flow disorders in all critical conditions go through 4 stages. Stage 1- spasm of resistance vessels and changes in the rheological properties of blood. Stress factors (hypoxia, fear, pain, trauma, etc.) lead to hypercatecholaminemia, which causes primary spasm of arterioles to centralize blood flow in case of blood loss or a decrease in cardiac output of any etiology (myocardial infarction, hypovolemia in peritonitis, acute intestinal obstruction, burns, etc.) .d.). Narrowing of arterioles reduces the rate of blood flow in the capillary, which changes the rheological properties of the blood and leads to aggregation of sludge cells. This begins the 2nd stage of microcirculation disorders, at which the following phenomena occur: a) tissue ischemia occurs, which leads to an increase in the concentration of acid metabolites, active polypeptides. However, the sludge phenomenon is characterized by the fact that the flows are stratified and the plasma flowing from the capillary can carry acidic metabolites and aggressive metabolites into the general circulation. Thus, the functional ability of the organ where microcirculation was disturbed is sharply reduced. b) fibrin settles on erythrocyte aggregates, as a result of which conditions arise for the development of DIC. c) aggregates of erythrocytes, enveloped by plasma substances, accumulate in the capillary and are switched off from the bloodstream - blood sequestration occurs. Sequestration differs from deposition in that in the "depot" the physico-chemical properties are not violated and the blood ejected from the depot is included in the bloodstream, completely physiologically suitable. Sequestered blood, on the other hand, must pass through a lung filter before it can again meet physiological parameters. If the blood is sequestered in a large number of capillaries, then its volume decreases accordingly. Therefore, hypovolemia occurs in any critical condition, even in those that are not accompanied by primary blood or plasma loss. II stage rheological disorders - a generalized lesion of the microcirculation system. Before other organs, the liver, kidneys, and pituitary gland suffer. The brain and myocardium are the last to suffer. After blood sequestration has already reduced the minute volume of blood, hypovolemia, with the help of additional arteriolospasm aimed at centralizing blood flow, includes new microcirculation systems in the pathological process - the volume of sequestered blood increases, as a result of which BCC drops. Stage III- total damage to blood circulation, metabolic disorders, disruption of metabolic systems. Summing up the above, it is possible to distinguish 4 stages for any violation of blood flow: violation of the rheological properties of blood, blood sequestration, hypovolemia, generalized damage to microcirculation and metabolism. Moreover, in the thanatogenesis of the terminal state, it does not matter what was primary: a decrease in BCC due to blood loss or a decrease in cardiac output due to right ventricular failure (acute myocardial infarction). in the event of the above vicious circle, the result of hemodynamic disturbances is in principle the same. The simplest criteria for microcirculation disorders can be: a decrease in diuresis to 0.5 ml / min or less, the difference between the skin and rectal temperatures is more than 4 degrees. C, the presence of metabolic acidosis and a decrease in the arterio-venous oxygen difference are a sign that the latter is not absorbed by the tissues.

Conclusion

The cardiac muscle, like any other muscle, has a number of physiological properties: excitability, conductivity, contractility, refractoriness and automaticity.

For the viscosity properties of blood, the protein composition of the plasma is important. Thus, albumins reduce the viscosity and ability of cells to aggregate, while globulins act in the opposite way. Fibrinogen is especially active in increasing the viscosity and tendency of cells to aggregate, the level of which changes under any stressful conditions. Hyperlipidemia and hypercholesterolemia also contribute to the violation of the rheological properties of the blood.

Bibliography:

1) S.A. Georgieva and others. Physiology. - M.: Medicine, 1981.

2) E.B. Babsky, G.I. Kositsky, A.B. Kogan and others. Human Physiology. - M.: Medicine, 1984

3) Yu.A. Ermolaev Age physiology. - M .: Higher. School, 1985

4) S.E. Sovetov, B.I. Volkov and others. School hygiene. - M .: Education, 1967

5) "Emergency Medical Care", ed. J. E. Tintinalli, Rl. Crouma, E. Ruiz, Translated from English by Dr. med. Sciences V.I.Kandrora, MD M.V. Neverova, Dr. med. Sciences A.V. Suchkova, Ph.D. A.V.Nizovoy, Yu.L.Amchenkov; ed. MD V.T. Ivashkina, D.M.N. P.G. Bryusov; Moscow "Medicine" 2001

6) Intensive therapy. Resuscitation. First Aid: Textbook / Ed. V.D. Malyshev. - M.: Medicine. - 2000. - 464 p.: ill. - Proc. lit. For students of the system of postgraduate education.- ISBN 5-225-04560-X

Currently, the problem of microcirculation attracts great attention of theorists and clinicians. Unfortunately, the accumulated knowledge in this area has not yet been properly applied in the practice of a doctor due to the lack of reliable and affordable diagnostic methods. However, without understanding the basic patterns of tissue circulation and metabolism, it is impossible to correctly use modern means of infusion therapy.

The microcirculation system plays an extremely important role in providing tissues with blood. This occurs mainly due to the reaction of vasomotion, which is carried out by vasodilators and vasoconstrictors in response to changes in tissue metabolism. The capillary network makes up 90% of the circulatory system, but 60-80% of it remains inactive.

The microcirculatory system forms a closed blood flow between arteries and veins (Fig. 3). It consists of arterpoles (diameter 30-40 µm), which end in terminal arterioles (20-30 µm), which divide into many metarterioles and precapillaries (20-30 µm). Further, at an angle close to 90°, rigid tubes devoid of a muscular membrane diverge, i.e. true capillaries (2-10 microns).

Rice. 3. A simplified diagram of the distribution of blood vessels in the microcirculation system 1 - artery; 2 - thermal artery; 3 - arterrol; 4 - terminal arteriole; 5 - metarteril; 6 - precapillary with muscle pulp (sphincter); 7 - capillary; 8 - collective venule; 9 - venule; 10 - vein; 11 - main channel (central trunk); 12 - arteriolo-venular shunt.

Metatereriols at the level of precapillaries have muscle clamps that regulate the flow of blood into the capillary bed and at the same time create the peripheral resistance necessary for the work of the heart. Precapillaries are the main regulatory link of microcirculation, providing the normal function of macrocirculation and transcapillary exchange. The role of precapillaries as regulators of microcirculation is especially important in various volemia disorders, when the level of BCC depends on the state of transcapillary metabolism.

The continuation of metarteriol forms the main channel (central trunk), which passes into the venous system. The collecting veins, which depart from the venous section of the capillaries, also join here. They form prevenules, which have muscular elements and are able to block the flow of blood from the capillaries. The prevenules assemble into venules and form a vein.

Between arterioles and venules there is a bridge - an arteriole-venous shunt, which is actively involved in the regulation of blood flow through microvessels.

The structure of the bloodstream. The blood flow in the microcirculation system has a certain structure, which is determined primarily by the speed of blood movement. In the center of the blood flow, creating an axial line, erythrocytes are located, which, together with the plasma, move one after the other at a certain interval. This flow of red blood cells creates an axis around which other cells - white blood cells and platelets - are located. The erythrocyte current has the highest advance rate. Platelets and leukocytes located along the vessel wall move more slowly. The arrangement of the components of the blood is quite definite and does not change at a normal blood flow velocity.

Directly in the true capillaries, the blood flow is different, since the diameter of the capillaries (2-10 microns) is less than the diameter of the erythrocytes (7-8 microns). In these vessels, the entire lumen is occupied mainly by erythrocytes, which acquire an elongated configuration in accordance with the lumen of the capillary. The near-wall plasma layer is preserved. It is necessary as a lubricant for the sliding of the red blood cell. The plasma also retains the electrical potential of the erythrocyte membrane and its biochemical properties, on which the elasticity of the membrane itself depends. In the capillary, the blood flow has a laminar character, its speed is very low - 0.01-0.04 cm / s at an arterial pressure of 2-4 kPa (15-30 mm Hg).

Rheological properties of blood. Rheology is the science of the fluidity of liquid media. It studies mainly laminar flows, which depend on the relationship of inertial forces and viscosity.

Water has the lowest viscosity, allowing it to flow under all conditions, regardless of the flow rate and temperature factor. Non-Newtonian fluids, which include blood, do not obey these laws. The viscosity of water is a constant value. Blood viscosity depends on a number of physicochemical parameters and varies widely.

Depending on the diameter of the vessel, the viscosity and fluidity of the blood change. The Reynolds number reflects the feedback between the viscosity of the medium and its fluidity, taking into account the linear forces of inertia and the diameter of the vessel. Microvessels with a diameter of no more than 30-35 microns have a positive effect on the viscosity of the blood flowing in them and its fluidity increases as it penetrates into narrower capillaries. This is especially pronounced in capillaries having a diameter of 7-8 microns. However, in smaller capillaries, the viscosity increases.

The blood is in constant motion. This is its main characteristic, its function. As the blood flow velocity increases, the viscosity of the blood decreases and, conversely, when the blood flow slows down, it increases. However, there is also an inverse relationship: the blood flow velocity is determined by the viscosity. To understand this purely rheological effect, one should consider the blood viscosity index, which is the ratio of shear stress to shear rate.

The blood flow consists of layers of fluid that move in parallel in it, and each of them is under the influence of a force that determines the shift (“shear stress”) of one layer in relation to another. This force is created by systolic blood pressure.

The concentration of the ingredients contained in it - erythrocytes, nuclear cells, fatty acid proteins, etc. - has a certain effect on blood viscosity.

Red blood cells have an intrinsic viscosity, which is determined by the viscosity of the hemoglobin they contain. The internal viscosity of an erythrocyte can vary widely, which determines its ability to penetrate into narrower capillaries and take an elongated shape (thixitropy). Basically, these properties of the erythrocyte are determined by the content of phosphorus fractions in it, in particular ATP. Hemolysis of erythrocytes with the release of hemoglobin into plasma increases the viscosity of the latter by 3 times.

For the characterization of blood viscosity, proteins are extremely important. A direct dependence of blood viscosity on the concentration of blood proteins was revealed, especially a 1 -, a 2 -, beta and gamma globulins, as well as fibrinogen. Albumin plays a rheologically active role.

Other factors that actively affect blood viscosity include fatty acids, carbon dioxide. Normal blood viscosity averages 4-5 cP (centipoise).

Blood viscosity, as a rule, is increased in shock (traumatic, hemorrhagic, burn, toxic, cardiogenic, etc.), dehydration, erythrocythemia, and a number of other diseases. In all these conditions, microcirculation suffers first of all.

To determine the viscosity, there are capillary-type viscometers (Oswald designs). However, they do not meet the requirement for determining the viscosity of moving blood. In this regard, viscometers are currently being designed and used, which are two cylinders of different diameters, rotating on the same axis; blood circulates in the gap between them. The viscosity of such blood should reflect the viscosity of the blood circulating in the vessels of the patient's body.

The most severe violation of the structure of capillary blood flow, fluidity and viscosity of blood occurs due to aggregation of erythrocytes, i.e. gluing of red cells together with the formation of "coin columns" [Chizhevsky A.L., 1959]. This process is not accompanied by hemolysis of erythrocytes, as with agglutination of an immunobiological nature.

The mechanism of erythrocyte aggregation may be related to plasma, erythrocyte, or hemodynamic factors.

Of the plasma factors, the main role is played by proteins, especially those with high molecular weight, which violate the ratio of albumin and globulins. A 1 -, a 2 - and beta-globulin fractions, as well as fibrinogen, have a high aggregation ability.

Violations of the properties of erythrocytes include a change in their volume, internal viscosity with a loss of membrane elasticity and the ability to penetrate into the capillary bed, etc.

Deceleration of blood flow velocity is often associated with a decrease in shear rate, i.e. occurs when blood pressure falls. Erythrocyte aggregation is observed, as a rule, with all types of shock and intoxication, as well as with massive blood transfusions and inadequate cardiopulmonary bypass [Rudaev Ya.A. et al., 1972; Solovyov G.M. et al., 1973; Gelin L. E., 1963, etc.].

Generalized aggregation of erythrocytes is manifested by the phenomenon of "sludge". The name of this phenomenon was suggested by M.N. Knisely, "sludging", in English "swamp", "dirt". Aggregates of erythrocytes undergo resorption in the reticuloendothelial system. This phenomenon always causes a difficult prognosis. It is necessary to use disaggregation therapy as soon as possible using low molecular weight solutions of dextran or albumin.

The development of "sludge" in patients can be accompanied by a very misleading pinking (or redness) of the skin due to the accumulation of sequestered erythrocytes in non-functioning subcutaneous capillaries. This clinical picture is "sludge", i.e. the last degree of development of erythrocyte aggregation and impaired capillary blood flow is described by L.E. Gelin in 1963 under the name "red shock" ("red shock"). The patient's condition is extremely severe and even hopeless, unless sufficiently intensive measures are taken.