Management of rheological properties of blood. Rheological properties of blood. Violation of blood rheology

The area of ​​mechanics that studies the features of deformation and flow of real continuous media, one of the representatives of which are non-Newtonian fluids with structural viscosity, is rheology. In this article, consider the rheological properties will become clear.

Definition

A typical non-Newtonian fluid is blood. It is called plasma if it is devoid of formed elements. Serum is plasma that does not contain fibrinogen.

Hemorheology, or rheology, studies mechanical patterns, especially how the physical and colloidal properties of blood change during circulation at different speeds and in different parts of the vascular bed. Its properties, the bloodstream, the contractility of the heart determine the movement of blood in the body. When the linear flow velocity is low, the blood particles move parallel to the axis of the vessel and towards each other. In this case, the flow has a layered character, and the flow is called laminar. So what are rheological properties? More on this later.

What is the Reynolds number?

In the case of an increase in the linear velocity and exceeding a certain value, which is different for all vessels, the laminar flow will turn into a vortex, chaotic, called turbulent. The rate of transition from laminar to turbulent motion determines the Reynolds number, which is approximately 1160 for blood vessels. According to Reynolds numbers, turbulence can only occur in those places where large vessels branch, as well as in the aorta. In many vessels, the fluid moves laminar.

Shear rate and stress

Not only the volumetric and linear velocity of blood flow is important, two more important parameters characterize the movement to the vessel: velocity and shear stress. Shear stress characterizes the force acting on a unit vascular surface in a tangential direction to the surface, measured in pascals or dynes/cm 2 . The shear rate is measured in reciprocal seconds (s-1), which means it is the magnitude of the gradient of the velocity of movement between layers of fluid moving in parallel per unit distance between them.

On what parameters do rheological properties depend?

The ratio of stress to shear rate determines blood viscosity, measured in mPas. For a solid fluid, the viscosity depends on the shear rate range of 0.1-120 s-1. If the shear rate is >100 s-1, the viscosity changes not so pronounced, and after reaching the shear rate of 200 s-1, it almost does not change. The value measured at high shear rate is called asymptotic. The principal factors that affect viscosity are the deformability of cell elements, hematocrit and aggregation. And given the fact that there are much more red blood cells compared to platelets and white blood cells, they are mainly determined by red cells. This is reflected in the rheological properties of blood.

Viscosity Factors

The most important factor determining viscosity is the volume concentration of red blood cells, their average volume and content, this is called hematocrit. It is approximately 0.4-0.5 l / l and is determined by centrifugation from a blood sample. Plasma is a Newtonian fluid, the viscosity of which determines the composition of proteins, and it depends on temperature. Viscosity is most affected by globulins and fibrinogen. Some researchers believe that a more important factor that leads to a change in plasma viscosity is the ratio of proteins: albumin / fibrinogen, albumin / globulins. The increase occurs during aggregation, determined by the non-Newtonian behavior of whole blood, which determines the aggregation ability of red blood cells. Physiological aggregation of erythrocytes is a reversible process. That's what it is - the rheological properties of blood.

The formation of aggregates by erythrocytes depends on mechanical, hemodynamic, electrostatic, plasma and other factors. Nowadays, there are several theories that explain the mechanism of erythrocyte aggregation. The most well-known today is the theory of the bridging mechanism, according to which bridges from large molecular proteins, fibrinogen, Y-globulins are adsorbed on the surface of erythrocytes. The net aggregation force is the difference between the shear force (causes disaggregation), the electrostatic repulsion layer of erythrocytes, which are negatively charged, the force in the bridges. The mechanism responsible for the fixation of negatively charged macromolecules on erythrocytes, that is, Y-globulin, fibrinogen, is not yet fully understood. There is an opinion that the molecules are linked due to the dispersed van der Waals forces and weak hydrogen bonds.

What helps to evaluate the rheological properties of blood?

Why does erythrocyte aggregation occur?

Explanation of erythrocyte aggregation is also explained by depletion, the absence of high-molecular proteins close to erythrocytes, and therefore a pressure interaction appears, which is similar in nature to the osmotic pressure of a macromolecular solution, leading to the convergence of suspended particles. In addition, there is a theory linking erythrocyte aggregation with erythrocyte factors, leading to a decrease in the zeta potential and a change in the metabolism and shape of erythrocytes.

Due to the relationship between the viscosity and aggregation ability of erythrocytes, in order to assess the rheological properties of blood and the features of its movement through the vessels, it is necessary to conduct a comprehensive analysis of these indicators. One of the most common and quite accessible methods for measuring aggregation is the assessment of the rate of erythrocyte sedimentation. However, the traditional version of this test is not very informative, since it does not take into account rheological characteristics.

Measurement methods

According to studies of rheological blood characteristics and factors that affect them, it can be concluded that the assessment of the rheological properties of blood is affected by the aggregation state. Nowadays, researchers pay more attention to the study of the microrheological properties of this liquid, however, viscometry has also not lost its relevance. The main methods for measuring the properties of blood can be divided into two groups: with a homogeneous stress and strain field - cone plane, disk, cylindrical and other rheometers with different geometry of the working parts; with a relatively inhomogeneous field of deformations and stresses - according to the registration principle of acoustic, electrical, mechanical vibrations, devices that work according to the Stokes method, capillary viscometers. This is how the rheological properties of blood, plasma and serum are measured.

Two types of viscometers

The most widespread now are two types and capillary. Viscometers are also used, the inner cylinder of which floats in the liquid being tested. Now they are actively engaged in various modifications of rotational rheometers.

Conclusion

It is also worth noting that the noticeable progress in the development of rheological technology just makes it possible to study the biochemical and biophysical properties of blood in order to control microregulation in metabolic and hemodynamic disorders. Nevertheless, the development of methods for the analysis of hemorheology, which would objectively reflect the aggregation and rheological properties of the Newtonian fluid, is currently relevant.

Ministry of Education of the Russian Federation

Penza State University

Medical Institute

Department of Therapy

Head department of d.m.s.

"RHEOLOGICAL PROPERTIES OF BLOOD AND THEIR DISORDERS DURING INTENSIVE CARE"

Completed: 5th year student

Checked by: Ph.D., Associate Professor

Penza

Plan

Introduction

1. Physical basis of hemorheology

2. The reason for the "non-Newtonian behavior" of blood

3. Main determinants of blood viscosity

4. Hemorheological disorders and venous thrombosis

5. Methods for studying the rheological properties of blood

Literature

Introduction

Hemorheology studies the physical and chemical properties of blood, which determine its fluidity, i.e. the ability to reversible deformation under the action of external forces. The generally accepted quantitative measure of the fluidity of blood is its viscosity.

Deterioration of blood flow is typical for patients in the intensive care unit. Increased blood viscosity creates additional resistance to blood flow and is therefore associated with excessive cardiac afterload, microcirculatory disorders, and tissue hypoxia. With a hemodynamic crisis, blood viscosity also increases due to a decrease in blood flow velocity. A vicious circle ensues that maintains stasis and shunting of blood in the microvasculature.

Disorders in the hemorheology system are a universal mechanism for the pathogenesis of critical conditions, therefore, optimization of the rheological properties of blood is the most important tool in intensive care. A decrease in blood viscosity helps to accelerate blood flow, increase DO 2 to tissues, and facilitate the work of the heart. With the help of rheologically active agents, it is possible to prevent the development of thrombotic, ischemic and infectious complications of the underlying disease.

Applied hemorheology is based on a number of physical principles of blood flow. Their understanding helps to choose the optimal method of diagnosis and treatment.

1. Physical basis of hemorheology

Under normal conditions, a laminar type of blood flow is observed in almost all parts of the circulatory system. It can be represented as an infinite number of fluid layers that move in parallel without mixing with each other. Some of these layers are in contact with a fixed surface - the vascular wall, and their movement, accordingly, slows down. Neighboring layers still tend in the longitudinal direction, but slower near-wall layers delay them. Inside the flow, friction occurs between the layers. A parabolic velocity distribution profile appears with a maximum at the center of the vessel. The near-wall liquid layer can be considered immovable. The viscosity of a simple fluid remains constant (8 s. Poise), and the viscosity of the blood varies depending on the conditions of blood flow (from 3 to 30 s Poise).

The property of blood to provide "internal" resistance to those external forces that set it in motion is called viscosity η . Viscosity is due to the forces of inertia and cohesion.

At a hematocrit of 0, blood viscosity approaches that of plasma.

For the correct measurement and mathematical description of viscosity, concepts such as shear stress are introduced. With and shear rate at . The first indicator is the ratio of the friction force between adjacent layers to their area - F / S . It is expressed in dynes / cm 2 or pascals *. The second indicator is the layer velocity gradient - delta V / L . It is measured in s -1 .

According to Newton's equation, the shear stress is directly proportional to the shear rate: τ= η·γ. This means that the greater the difference in velocity between layers of fluid, the greater their friction. Conversely, the equalization of the velocity of the liquid layers reduces the mechanical stress along the watershed line. Viscosity in this case acts as a proportionality factor.

The viscosity of simple, or Newtonian, liquids (for example, water) is constant under any conditions of motion, i.e. there is a linear relationship between shear stress and shear rate for these fluids.

Unlike simple liquids, blood is able to change its viscosity with a change in the speed of blood flow. So, in the aorta and the main arteries, the blood viscosity approaches 4-5 relative units (if we take the viscosity of water at 20 ° C as a reference measure). In the venous part of the microcirculation, despite the low shear stress, the viscosity increases 6-8 times relative to its level in the artery (ie, up to 30-40 relative units). At extremely low, non-physiological shear rates, blood viscosity can increase by a factor of 1000 (!).

Thus, the relationship between shear stress and shear rate for whole blood is non-linear, exponential. This "rheological behavior of blood"* is called "non-Newtonian".

2. The reason for the "non-Newtonian behavior" of blood

The "non-Newtonian behavior" of blood is due to its roughly dispersed nature. From a physicochemical point of view, blood can be represented as a liquid medium (water) in which a solid, insoluble phase (blood cells and macromolecular substances) is suspended. The particles of the dispersed phase are large enough to resist Brownian motion. Therefore, a common property of such systems is their nonequilibrium. The components of the dispersed phase are constantly striving to isolate and precipitate cell aggregates from the dispersed medium.

The main and rheologically most significant type of cellular aggregates of blood is erythrocyte. It is a multidimensional cellular complex with a typical "coin column" shape. Its characteristic features are the reversibility of the connection and the absence of functional activation of cells. The structure of the erythrocyte aggregate is maintained mainly by globulins. It is known that the erythrocytes of a patient with an initially increased rate of sedimentation after their addition to the single-group plasma of a healthy person begin to settle at a normal rate. Conversely, if the erythrocytes of a healthy person with a normal sedimentation rate are placed in the patient's plasma, then their precipitation will be significantly accelerated.

Fibrinogen is a natural inducer of aggregation. The length of its molecule is 17 times its width. Due to this asymmetry, fibrinogen is able to spread in the form of a "bridge" from one cell membrane to another. The bond formed in this case is fragile and breaks under the action of a minimum mechanical force. They operate in the same way a 2 - and beta-macroglobulins, fibrinogen degradation products, immunoglobulins. A closer approach of erythrocytes and their irreversible binding to each other is prevented by a negative membrane potential.

It should be emphasized that erythrocyte aggregation is a rather normal process than a pathological one. Its positive side is to facilitate the passage of blood through the microcirculation system. As aggregates form, the surface-to-volume ratio decreases. As a result, the resistance of the aggregate to friction is much less than the resistance of its individual components.

3. Main determinants of blood viscosity

Blood viscosity is influenced by many factors. All of them realize their action by changing the viscosity of the plasma or the rheological properties of blood cells.

Content of erythrocytes. Erythrocyte is the main cell population of the blood, actively participating in the processes of physiological aggregation. For this reason, changes in hematocrit (Ht) significantly affect blood viscosity. So, with an increase in Ht from 30 to 60%, the relative blood viscosity doubles, and with an increase in Ht from 30 to 70%, it triples. Hemodilution, on the other hand, reduces blood viscosity.

The term "rheological behavior of blood" (rheologicalbehavior) is generally accepted, emphasizing the "non-Newtonian" nature of blood fluidity.

Deformation ability of erythrocytes. The diameter of the erythrocyte is approximately 2 times the lumen of the capillary. Because of this, the passage of an erythrocyte through the microvasculature is possible only if its volumetric configuration changes. Calculations show that if the erythrocyte was not capable of deformation, then the blood with Ht 65% would turn into a dense homogeneous formation and the blood flow would stop completely in the peripheral parts of the circulatory system. However, due to the ability of erythrocytes to change their shape and adapt to environmental conditions, blood circulation does not stop even at Ht 95-100%.

There is no coherent theory of the deformation mechanism of erythrocytes. Apparently, this mechanism is based on the general principles of the transition of a sol into a gel. It is assumed that the deformation of erythrocytes is an energy-dependent process. Perhaps hemoglobin A takes an active part in it. It is known that the content of hemoglobin A in the erythrocyte decreases in some hereditary blood diseases (sickle cell anemia), after operations under cardiopulmonary bypass. This changes the shape of erythrocytes and their plasticity. Observe increased blood viscosity, which does not correspond to low Ht.

Plasma viscosity. Plasma as a whole can be referred to the category of "Newtonian" liquids. Its viscosity is relatively stable in various parts of the circulatory system and is mainly determined by the concentration of globulins. Among the latter, fibrinogen is of primary importance. It is known that the removal of fibrinogen reduces the viscosity of plasma by 20%, so the viscosity of the resulting serum approaches the viscosity of water.

Normally, plasma viscosity is about 2 rel. units This is approximately 1/15 of the internal resistance that develops with whole blood in the venous microcirculation section. Nevertheless, plasma has a very significant effect on peripheral blood flow. In capillaries, blood viscosity is reduced by half compared with proximal and distal vessels of larger diameter (phenomenon §). Such a "prolapse" of viscosity is associated with the axial orientation of erythrocytes in a narrow capillary. In this case, the plasma is pushed to the periphery, to the wall of the vessel. It serves as a "lubricant" that ensures the chain of blood cells slides with minimal friction.

This mechanism functions only with a normal protein composition of the plasma. An increase in the level of fibrinogen or any other globulin leads to difficulty in capillary blood flow, sometimes of a critical nature. Thus, myeloma, Waldenström's macroglobulinemia and some collagenoses are accompanied by excessive production of immunoglobulins. The viscosity of the plasma in this case increases relative to the normal level by 2-3 times. Symptoms of severe microcirculation disorders begin to predominate in the clinical picture: decreased vision and hearing, drowsiness, weakness, headache, paresthesia, bleeding of mucous membranes.

Pathogenesis of hemorheological disorders. In the practice of intensive care, hemorheological disorders occur under the influence of a complex of factors. The action of the latter in a critical situation is universal.

biochemical factor. On the first day after surgery or injury, the level of fibrinogen usually doubles. The peak of this increase falls on the 3-5th day, and the normalization of the fibrinogen content occurs only by the end of the 2nd postoperative week. In addition, fibrinogen degradation products, activated platelet procoagulants, catecholamines, prostaglandins, and lipid peroxidation products appear in the bloodstream in excess. All of them act as inducers of red blood cell aggregation. A peculiar biochemical situation is formed - "rheotoxemia".

hematological factor. Surgical intervention or trauma is also accompanied by certain changes in the cellular composition of the blood, which are called hematological stress syndrome. Young granulocytes, monocytes and platelets of increased activity enter the bloodstream.

hemodynamic factor. The increased aggregation tendency of blood cells under stress is superimposed on local hemodynamic disturbances. It has been shown that with uncomplicated abdominal interventions, the volumetric blood flow velocity through the popliteal and iliac veins drops by 50%. This is due to the fact that immobilization of the patient and muscle relaxants block the physiological mechanism of the “muscle pump” during the operation. In addition, under the influence of mechanical ventilation, anesthetics or blood loss, systemic pressure decreases. In such a situation, the kinetic energy of systole may not be enough to overcome the adhesion of blood cells to each other and to the vascular endothelium. The natural mechanism of hydrodynamic disaggregation of blood cells is disturbed, microcirculatory stasis occurs.

4. Hemorheological disorders and venous thrombosis

Slowing the speed of movement in the venous circulation provokes erythrocyte aggregation. However, the inertia of motion can be quite large and blood cells will experience an increased deformation load. Under its influence, ATP is released from erythrocytes - a powerful inducer of platelet aggregation. The low shear rate also stimulates the adhesion of young granulocytes to the wall of the venules (Farheus-Vejiens phenomenon). Irreversible aggregates are formed that can form the cell nucleus of a venous thrombus.

Further development of the situation will depend on the activity of fibrinolysis. As a rule, an unstable balance arises between the processes of formation and resorption of a thrombus. For this reason, most cases of deep vein thrombosis of the lower extremities in hospital practice are latent and resolve spontaneously, without consequences. The use of antiplatelet agents and anticoagulants is a highly effective way to prevent venous thrombosis.

5. Methods for studying the rheological properties of blood

The "non-Newtonian" nature of blood and the shear rate factor associated with it must necessarily be taken into account when measuring viscosity in clinical laboratory practice. Capillary viscometry is based on the flow of blood through a graduated vessel under the influence of gravity, and therefore is physiologically incorrect. Real blood flow conditions are simulated on a rotational viscometer.

The fundamental elements of such a device include the stator and the rotor congruent to it. The gap between them serves as a working chamber and is filled with a blood sample. The fluid movement is initiated by the rotation of the rotor. It, in turn, is arbitrarily set in the form of a certain shear rate. The measured value is the shear stress, which occurs as a mechanical or electrical moment necessary to maintain the selected speed. Blood viscosity is then calculated using Newton's formula. The unit of measure for blood viscosity in the CGS system is Poise (1 Poise = 10 dyn x s/cm 2 = 0.1 Pa x s = 100 rel. units).

It is obligatory to measure blood viscosity in the range of low (<10 с -1) и высоких (>100 s -1) shear rates. The low range of shear rates reproduces the conditions of blood flow in the venous section of the microcirculation. The determined viscosity is called structural. It mainly reflects the tendency of erythrocytes to aggregate. High shear rates (200-400 s -1) are achieved in vivo in the aorta, main vessels and capillaries. At the same time, as rheoscopic observations show, erythrocytes occupy a predominantly axial position. They stretch in the direction of movement, their membrane begins to rotate relative to the cellular content. Due to hydrodynamic forces, almost complete disaggregation of blood cells is achieved. Viscosity, determined at high shear rates, depends mainly on the plasticity of erythrocytes and the shape of the cells. It's called dynamic.

As a standard for research on a rotational viscometer and the corresponding norm, you can use indicators according to the method of N.P. Alexandrova and others.

For a more detailed presentation of the rheological properties of blood, several more specific tests are carried out. The deformability of erythrocytes is estimated by the rate of passage of diluted blood through a microporous polymer membrane (d=2-8 μm). The aggregation activity of red blood cells is studied using nephelometry by changing the optical density of the medium after adding aggregation inducers (ADP, serotonin, thrombin or adrenaline) to it.

Diagnosis of hemorheological disorders . Disorders in the hemorheology system, as a rule, proceed latently. Their clinical manifestations are nonspecific and inconspicuous. Therefore, the diagnosis is determined for the most part by laboratory data. Its leading criterion is the value of blood viscosity.

The main direction of shifts in the hemorheology system in critically ill patients is the transition from increased blood viscosity to low. This dynamic, however, is accompanied by a paradoxical deterioration in blood flow.

Hyperviscosity Syndrome. It is non-specific and widely used in the clinic of internal diseases: in atherosclerosis, angina pectoris, chronic obstructive bronchitis, gastric ulcer, obesity, diabetes mellitus, obliterating endarteritis, etc. At the same time, a moderate increase in blood viscosity up to 35 cPais is noted at y=0, 6 s -1 and 4.5 cPas at y==150 s -1 . Microcirculatory disorders are usually mild. They progress only as the underlying disease develops. Hyperviscosity syndrome in patients admitted to the intensive care unit should be considered as a background condition.

Syndrome of low blood viscosity. As the critical state develops, blood viscosity decreases due to hemodilution. Viscometry indicators are 20-25 cPas at y=0.6 s -1 and 3-3.5 cPas at y=150 s -1 . Similar values ​​can be predicted from Ht, which usually does not exceed 30-35%. In the terminal state, the decrease in blood viscosity reaches the stage of "very low" values. Severe hemodilution develops. Ht decreases to 22-25%, dynamic blood viscosity - up to 2.5-2.8 cPas and structural blood viscosity - up to 15-18 cPas.

The low value of blood viscosity in a critically ill patient creates a misleading impression of hemorheological well-being. Despite hemodilution, microcirculation deteriorates significantly in low blood viscosity syndrome. The aggregation activity of red blood cells increases by 2-3 times, the passage of erythrocyte suspension through nucleopore filters slows down by 2-3 times. After recovery of Ht by hemoconcentration in vitro in such cases, blood hyperviscosity is detected.

Against the background of low or very low blood viscosity, massive erythrocyte aggregation may develop, which completely blocks the microvasculature. This phenomenon, described by M.N. Knisely in 1947 as a "sludge" phenomenon, indicates the development of a terminal and, apparently, an irreversible phase of a critical condition.

The clinical picture of low blood viscosity syndrome consists of severe microcirculatory disorders. Note that their manifestations are nonspecific. They may be due to other, non-rheological mechanisms.

Clinical manifestations of low blood viscosity syndrome:

Tissue hypoxia (in the absence of hypoxemia);

Increased OPSS;

Deep vein thrombosis of the extremities, recurrent pulmonary thromboembolism;

Adynamia, stupor;

Deposition of blood in the liver, spleen, subcutaneous vessels.

Prevention and treatment. Patients entering the operating room or intensive care unit need to optimize the rheological properties of the blood. This prevents the formation of venous blood clots, reduces the likelihood of ischemic and infectious complications, and facilitates the course of the underlying disease. The most effective methods of rheological therapy are blood dilution and suppression of the aggregation activity of its formed elements.

Hemodilution. The erythrocyte is the main carrier of structural and dynamic resistance to blood flow. Therefore, hemodilution is the most effective rheological agent. Its beneficial effect has long been known. For many centuries, bloodletting has been perhaps the most common method of treating diseases. The appearance of low molecular weight dextrans was the next step in the development of the method.

Hemodilution increases peripheral blood flow, but at the same time reduces the oxygen capacity of the blood. Under the influence of two multidirectional factors, DO 2 is ultimately formed in tissues. It can increase due to blood dilution or, conversely, significantly decrease under the influence of anemia.

The lowest possible Ht, which corresponds to a safe level of DO 2 , is called optimal. Its exact value is still the subject of debate. The quantitative ratios of Ht and DO 2 are well known. However, it is not possible to assess the contribution of individual factors: anemia tolerance, tissue metabolism intensity, hemodynamic reserve, etc. According to the general opinion, the goal of therapeutic hemodilution is Ht 30-35%. However, the experience of treating massive blood loss without blood transfusion shows that an even greater decrease in Ht to 25 and even 20% is quite safe from the point of view of tissue oxygen supply.

Currently, three methods are mainly used to achieve hemodilution.

Hemodilution in hypervolemia mode implies such a transfusion of fluid, which leads to a significant increase in BCC. In some cases, a short-term infusion of 1-1.5 liters of plasma substitutes precedes induction anesthesia and surgery, in other cases, requiring longer hemodilution, a decrease in Ht is achieved by a constant fluid load at the rate of 50-60 ml/kg of the patient's body weight per day. Decreased viscosity of whole blood is the main consequence of hypervolemia. The viscosity of plasma, the plasticity of erythrocytes and their tendency to aggregation do not change. The disadvantages of the method include the risk of volume overload of the heart.

Hemodilution in normovolemia mode was originally proposed as an alternative to heterologous transfusions in surgery. The essence of the method lies in the preoperative sampling of 400-800 ml of blood in standard containers with a stabilizing solution. Controlled blood loss, as a rule, is replenished simultaneously with the help of plasma substitutes at the rate of 1:2. With some modification of the method, it is possible to harvest 2-3 liters of autologous blood without any side hemodynamic and hematological consequences. The collected blood is then returned during or after the operation.

Normolemic hemodilution is not only a safe, but low-cost method of autodonation, which has a pronounced rheological effect. Along with a decrease in Ht and the viscosity of whole blood after exfusion, there is a persistent decrease in plasma viscosity and the aggregation ability of erythrocytes. The flow of fluid between the interstitial and intravascular spaces is activated, along with it, the exchange of lymphocytes and the flow of immunoglobulins from tissues increase. All this ultimately leads to a reduction in postoperative complications. This method can be widely used in planned surgical interventions.

Endogenous hemodilution develops with pharmacological vasoplegia. The decrease in Ht in these cases is due to the fact that a protein-depleted and less viscous fluid enters the vascular bed from the surrounding tissues. Epidural blockade, halogen-containing anesthetics, ganglion blockers and nitrates have a similar effect. The rheological effect accompanies the main therapeutic effect of these agents. The degree of decrease in blood viscosity is not predicted. It is determined by the current state of volume and hydration.

Anticoagulants. Heparin is obtained by extraction from biological tissues (lungs of cattle). The final product is a mixture of polysaccharide fragments with different molecular weights, but with similar biological activity.

The largest fragments of heparin in the complex with antithrombin III inactivate thrombin, while fragments of heparin with mol.m-7000 affect mainly the activated factor x.

Introduction in the early postoperative period of high molecular weight heparin at a dose of 2500-5000 IU under the skin 4-6 times a day has become a widespread practice. Such an appointment reduces the risk of thrombosis and thromboembolism by 1.5-2 times. Small doses of heparin do not prolong the activated partial thromboplastin time (APTT) and, as a rule, do not cause hemorrhagic complications. Heparin therapy along with hemodilution (intentional or incidental) are the main and most effective methods for the prevention of hemorheological disorders in surgical patients.

Low molecular weight fractions of heparin have a lower affinity for platelet von Willebrand factor. Because of this, they are even less likely to cause thrombocytopenia and bleeding compared to high molecular weight heparin. The first experience of using low molecular weight heparin (Clexane, Fraxiparin) in clinical practice gave encouraging results. Heparin preparations proved to be equipotential to traditional heparin therapy, and according to some data, even exceeded its preventive and therapeutic effect. In addition to safety, low molecular weight fractions of heparin are also characterized by economical administration (once a day) and the absence of the need to monitor aPTT. The choice of dose, as a rule, is carried out without taking into account body weight.

Plasmapheresis. The traditional rheological indication for plasmapheresis is the primary hyperviscosity syndrome, which is caused by excessive production of abnormal proteins (paraproteins). Their removal leads to a rapid regression of the disease. The effect, however, is short-lived. The procedure is symptomatic.

Currently, plasmapheresis is actively used for preoperative preparation of patients with obliterating diseases of the lower extremities, thyrotoxicosis, gastric ulcer, and purulent-septic complications in urology. This leads to an improvement in the rheological properties of blood, activation of microcirculation, and a significant reduction in the number of postoperative complications. They replace up to 1/2 of the volume of the OCP.

The decrease in globulin levels and plasma viscosity after a single plasmapheresis session can be significant, but short-lived. The main beneficial effect of the procedure, which extends to the entire postoperative period, is the so-called resuspension phenomenon. Washing of erythrocytes in a protein-free medium is accompanied by a stable improvement in the plasticity of erythrocytes and a decrease in their aggregation tendency.

Photomodification of blood and blood substitutes. With 2-3 procedures of intravenous blood irradiation with a helium-neon laser (wavelength 623 nm) of low power (2.5 mW), a distinct and prolonged rheological effect is observed. According to precision nephelometry, under the influence of laser therapy, the number of hyperergic reactions of platelets decreases, and the kinetics of their aggregation in vitro normalizes. The viscosity of the blood remains unchanged. UV rays (with a wavelength of 254-280 nm) in the extracorporeal circuit also have a similar effect.

The mechanism of the disaggregation action of laser and ultraviolet radiation is not entirely clear. It is believed that photomodification of blood first causes the formation of free radicals. In response, antioxidant defense mechanisms are activated, which block the synthesis of natural inducers of platelet aggregation (primarily prostaglandins).

Also proposed is ultraviolet irradiation of colloidal preparations (for example, rheopolyglucin). After their introduction, the dynamic and structural blood viscosity decreases by 1.5 times. Platelet aggregation is also significantly inhibited. Characteristically, unmodified rheopolyglucin is not able to reproduce all these effects.

Literature

1. "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

2. 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

1. Normalization of hemodynamics (restoration of blood flow velocity in the periphery);

2. Controlled hemodilution (blood thinning and viscosity reduction);

3. The introduction of antiplatelet agents and anticoagulants (prevention of thrombosis);

4. The use of drugs that reduce the rigidity of erythrocyte membranes;

5. Normalization of the acid-base state of the blood;

6. Normalization of the protein composition of the blood (introduction of albumin solutions).

For the purpose of hemodilution and disaggregation of cells, hemodez is used, as well as low molecular weight dextrans, which increase the electrostatic repulsion forces between shaped elements due to an increase in the negative charge on their surface, lower blood viscosity by attracting water into the vessels, cover the endothelium and vessels with a separating film, form complex compounds with fibrinogen, reduce the concentration of lipids.

Microcirculation disorders

In the organization of the circulatory system, one can distinguish the macrocirculation system - the heart pump, buffer vessels (arteries) and reservoir vessels (veins) - and the microcirculation system. The task of the latter is to connect the circulatory system to the general circulation of the body and distribute cardiac output between organs according to their needs. Therefore, each organ has its own microcirculation system inherent only to it, adequate to the function it performs. Nevertheless, it was possible to identify 3 main types of the structure of the terminal vascular bed (classical, bridge and network) and describe their structure.

The microcirculation system, schematically shown in Fig. 4, consists of the following microvessels:

arterioles (diameter 100 microns or less);

precapillary arterioles or precapillaries or metarterioles (diameter 25 - 10 microns);

capillaries (diameter 2 - 20 microns);

postcapillary venules or postcapillaries (diameter 15 - 20 microns);

venules (diameter up to 100 microns).

In addition to these vessels, arteriolo-venular anastomoses are also distinguished - direct fistulas between arterioles / arteries and venules / veins. Their diameter is from 30 to 500 microns, they are found in most organs.

Figure 4. Scheme of the microvasculature [according to Chambers, Zweifach, 1944].

The driving force of blood flow in the microcirculation system is perfusion pressure or arteriovenous pressure difference. Therefore, this pressure is determined by the levels of total arterial and venous pressure, and its value can be influenced by the work of the heart, total blood volume and total peripheral vascular resistance. The relationship between central and peripheral circulation is expressed by the formula Q =  P/ R, where Q is the intensity (volume velocity) of blood flow in the microcirculation system, P is the arteriovenous pressure difference, R is the peripheral (hydrodynamic) resistance in the given vascular bed. Changes in both P and R are leading in peripheral circulatory disorders. The smaller the value of peripheral resistance, the greater the intensity of blood flow; the greater the value of peripheral resistance, the lower the intensity of blood flow. The regulation of peripheral circulation and microcirculation in all organs is carried out by changing the resistance to current in their vascular system. An increase in blood viscosity increases hydrodynamic resistance and thus reduces the intensity of blood flow. The magnitude of the hydrodynamic resistance depends much more on the radius of the vessels: the hydrodynamic resistance is inversely proportional to vascular radius to the fourth power . It follows that changes in the area of ​​the lumen of the vessels (due to vasoconstriction or expansion) affect blood flow much more than factors such as viscosity or pressure changes.

The main regulators of microcirculation are adducting small arteries and arterioles. and arteriovenous anastomoses. As a result of the expansion of the afferent arterioles, 1) the blood flow velocity increases, 2) the intracapillary pressure increases, and 3) the number of functioning capillaries increases. The latter will also be determined by the opening of the precapillary sphincters - the relaxation of two or more smooth muscle cells at the beginning of the capillaries.

Figure 5 Scheme of the main vessels of the microvasculature [according to Mchedlishvili, 1958].

A - smooth muscle cells of microvessels with vasomotor innervation; B- main capillary; B - capillaries forming a network. AVA - arterial-venous anastomosis.

The lumen of microvessels can actively change only if there are smooth muscle elements in their structure. On fig. 5, the types of vessels that contain them are shaded. It follows that autonomic nerves innervate all blood vessels except capillaries. However, recent studies have shown the presence of areas of close relationship between the terminal nerve elements and capillaries. They are specialized extensions of axons near the capillary wall, similar to extensions in the region of axo-axonal synapses, i.e. form, in fact, "synapses along the way." It is likely that this non-synaptic type of signal transduction, which ensures the free diffusion of neurotransmitters towards microvessels, is the main mode of nervous regulation of capillaries. In this case, not one capillary is regulated, but the entire vascular locus. With electrical stimulation of nerves (afferent and efferent) or under the action of neurotransmitters, prostaglandins, histamine (including due to degranulation of mast cells), ATP, adrenaline, and other vasoactive substances appear in the tissue. As a result, the state of endothelial cells mainly changes, transendothelial transport increases, endothelial permeability and tissue trophism change. Thus, the mediation of the regulatory and trophic influence of nerves on tissues through the circulatory system is carried out not only by rough regulation of blood flow to the organ and its parts, but also by fine regulation of trophism itself through a change in the state of the microvessel wall. On the other hand, the materials presented show that innervation disorders relatively quickly lead to significant changes in the ultrastructure and capillary permeability. Therefore, microcirculatory disorders and, in particular, changes in vascular permeability should play an important role in the development of neurogenic dystrophies.

Changes in vascular tone or vascular sphincters may be due to nervous, humoral and local regulatory mechanisms (table 1).

Table 1.

Regulation of the microvascular bed

Note. The number of crosses indicates the degree of regulation.

Nervous regulation carried out by the autonomic nervous system. The vasomotor nerves are predominantly sympathetic department(less often - parasympathetic) and abundantly innervate the arterioles of the skin, kidneys and celiac region. In the brain and skeletal muscles, these vessels are relatively weakly innervated. The mediator in the synapses is norepinephrine, which always causes muscle contraction. The degree of contraction of the vascular muscles depends directly on the frequency of impulses. The resting vascular tone is maintained due to the constant flow of impulses through the vasomotor nerves at a frequency of 1-3 per second (the so-called tonic impulse). At a pulse frequency of only about 10 per second, maximum vasoconstriction is observed. That., an increase in impulses in the vasomotor nerves leads to vasoconstriction, and a decrease in vasodilation, and the latter is limited by the basal vascular tone (i.e., the tone that is observed in the absence of impulses in the vasoconstrictor nerves or when they are transected).

Parasympathetic cholinergic vasodilating fibers innervate the vessels of the external genital organs, small arteries of the pia mater of the brain.

The nervous mechanism is also revealed in the analysis of vasodilatation of the skin in response to mechanical or chemical irritation of the skin. It - axon reflex, carried out with the help of nociceptive (pain-conducting) nerve fibers and neuropeptides.

The sensitivity of muscle cells to vasoactive substances is different. Microvessels are 10-100 times more sensitive than large ones; precapillary sphincters turned out to be the most sensitive in relation to the action of both narrowing and expanding agents. It was found that a similar reactivity is observed in relation to electrical stimulation (table 2). Under conditions of pathology, the sensitivity of microvessels to vasoactive substances changes.

table 2

The reactivity gradient of the microcirculatory bed of the mesentery of rats

(after Zweifach, 1961)

The reactivity of microvessels is also not the same in various organs and tissues. This regularity is especially evident in relation to adrenaline (Table 3). Skin microvessels have the highest sensitivity to adrenaline.

Table 3

Reactivity of rat microvessels to nopogic concentration

adrenaline (by Zweifach, 1961)

In recent years, the fact of the existence in the same neuron of two or more (up to seven) neurotransmitters of different chemical nature and in different combinations has been proven. The wide, if not ubiquitous, prevalence of neuropeptides in autonomic nerves (e.g., neuropeptide Y, vasoactive intestinal peptide, substance P, etc.) supplying blood vessels has been well proven by numerous immunohistochemical studies and indicates a significant increase in the complexity of the mechanisms of nervous regulation of vascular tone. An even greater complication of these mechanisms is associated with the discovery of neuropeptides in the composition of sensitive nerve fibers supplying blood vessels, and their possible "effector" role in the regulation of vascular tone.

Humoral regulation carried out by hormones and chemicals released in the body. Vasopressin (antidiuretic hormone) and angiotensin II cause vasoconstriction. Kallidin and bradykinin - vasodilation. Adrenaline, secreted by the adrenal glands, can have both a vasoconstrictor and a vasodilator effect. The answer is determined by the number of - or -adrenergic receptors on the vascular muscle membrane. If -receptors predominate in the vessels, then adrenaline causes their narrowing, and if the majority are -receptors, then it causes expansion.

Local regulatory mechanisms provide metabolic autoregulation of the peripheral circulation. They adapt the local blood flow to the functional needs of the organ. At the same time, metabolic vasodilating effects dominate over the nervous vasoconstrictor effects and in some cases completely suppress them. They expand microvessels: lack of oxygen, metabolic products - carbon dioxide, an increase in H-ions, lactate, pyruvate, ADP, AMP and adenosine, many mediators of damage or inflammation - histamine, bradykinin, prostaglandins A and E and substance P. It is believed that expansion with The action of some mediators occurs due to the release of nitric oxide from endothelial cells, which directly relaxes smooth muscles. Damage mediators narrow the microvessels - serotonin, prostaglandins F, thromboxane and endothelins.

With regard to the ability of capillaries to actively constrict, the answer is rather negative, since there are no smooth muscle cells. Those researchers who observe an active narrowing of their lumen explain this narrowing by contraction of the endotheliocyte in response to a stimulus and protrusion of the cell nucleus into the capillary. Passive narrowing or even complete closure of the capillary occurs when the tension of their walls prevails over intravascular pressure. This condition occurs when there is a decrease in blood flow through the adductor arteriole. A significant expansion of the capillaries is also difficult, since 95% of the elasticity of their walls falls on the connective substance surrounding them. Only when it is destroyed, for example, by inflammatory exudate, the increased intracapillary pressure can cause stretching of the capillary walls and their significant expansion.

In the arterial bed, pressure fluctuations are observed in accordance with the cardiac cycle. The amplitude of pressure fluctuation is called pulse pressure. In the terminal branches of the arteries and arterioles, the pressure drops sharply over several millimeters of the vascular network, reaching 30-35 mm Hg. at the end of arterioles. This is due to the high hydrodynamic resistance of these vessels. At the same time, pulse pressure fluctuations significantly decrease or disappear and the pulsating blood flow is gradually replaced by a continuous one (with a significant expansion of blood vessels, for example, during inflammation, pulse fluctuations are observed even in capillaries and small veins). Nevertheless, in arterioles, metarterioles, and precapillaries, rhythmic fluctuations in blood flow velocity can be noted. The frequency and amplitude of these fluctuations can be different, and they do not participate in the adaptation of the blood flow to the needs of the tissues. It is assumed that this phenomenon - endogenous vasomotor - is due to the automaticity of contractions of smooth muscle fibers and does not depend on autonomic nervous influences.

It is possible that changes in blood flow in the capillaries also depend on leukocytes. Leukocytes, unlike erythrocytes, are not disc-shaped, but spherical, and with a diameter of 6-8 microns, their volume exceeds the volume of erythrocytes by 2-3 times. When a leukocyte enters a capillary, it "gets stuck" at the mouth of the capillary for a while. According to researchers, it ranges from 0.05 seconds to several seconds. At this moment, the movement of blood in this capillary stops, and after slipping of the leukocyte into the microvessel, it is restored again.

The main forms of peripheral circulatory and microcirculation disorders are: 1. arterial hyperemia, 2. venous hyperemia, 3. ischemia, 4. stasis.

Thrombosis and embolism, which are not independent disorders of the microcirculation, appearing in this system, causing its serious violations.

Rheology is the science of flow and deformation.

The rheological properties of blood depend on:

1. Hemodynamic parameters - changes in the properties of blood during its movement. Hemodynamic parameters are determined by the propulsive ability of the heart, the functional state of the bloodstream and the properties of the blood itself.

2. Cellular factors (quantity, concentration - hematocrit, deformability, shape, functional state).

3. Plasma factors - the content of albumins, globulins, fibrinogen, FFA, TT, cholesterol, pH, electrolytes.

4. Interaction factors - intravascular aggregation of formed elements.

In the blood, a dynamic process of "aggregation - disaggregation" is constantly taking place. Normally, disaggregation dominates over aggregation. The resulting direction of the process "aggregation - disaggregation" is determined by the interaction of the following factors: hemodynamic, plasma, electrostatic, mechanical and conformational.

The hemodynamic factor determines the shear stress and the distance between individual cells in a stream.

Plasma and electrostatic factors determine the bridging and electrostatic mechanisms.

The bridging mechanism consists in the fact that the connecting element in the aggregate between erythrocytes are macromolecular compounds, the ends of the molecules of which, adsorbed on neighboring cells, form a kind of bridges. The distance between erythrocytes in the aggregate is proportional to the length of the binding molecules. The main plastic material for intererythrocyte bridges are fibrinogen and globulins. A necessary condition for the implementation of the bridge mechanism is the convergence of erythrocytes at a distance not exceeding the length of one macromolecule. It depends on the hematocrit. The electrostatic mechanism is determined by the charge on the surface of red blood cells. With acidosis, accumulation of lactate, (-) potential decreases and cells do not repel each other.

The gradual elongation and branching of the aggregate triggers the conformational mechanism and the aggregates form a three-dimensional spatial structure.

5. External conditions - temperature. As temperature increases, blood viscosity decreases.

Among intravascular disorders of microcirculation, one of the first places should be aggregation of erythrocytes and other blood cells.

The founders of the doctrine of "sludge", i.e. state of the blood, which is based on erythrocyte aggregation, are Knisese (1941) and his student Blosh. The term “slug” itself, literally translated from English, means “thick mud”, “mud”, “silt”. First of all, it is necessary to distinguish between the aggregation of blood cells (primarily erythrocytes) and agglutination of erythrocytes. The first process is reversible, while the second always seems to be irreversible, mainly associated with immune phenomena. Sludge development is an extreme degree of expression of aggregation of blood cells. Sludged blood has a number of differences from normal. The main features of smoothed blood should be considered as the adhesion of erythrocytes, leukocytes or platelets to each other and an increase in blood viscosity. This leads to such a state of the blood, which makes it very difficult to perfuse through the microvessels.

There are several types of sludge depending on the structural features of the aggregate.

I. Classical type. It is characterized by relatively large aggregates and dense packing of erythrocytes and with uneven contours. This type of sludge develops when an obstruction (such as a ligature) interferes with the free movement of blood through a vessel.

II. dextran type. The aggregates have different sizes, dense packing, rounded outlines, free spaces in the aggregates in the form of cavities. This type of sludge develops when dextran with a molecular weight of 250-500 and above KDn is introduced into the blood.

III. amorphous type. This type is characterized by the presence of a huge number of small aggregates similar to granules. In this case, the blood takes the form of a coarse liquid. The amorphous type of sludge develops with the introduction of ethyl, ADP and ATP, thrombin, serotonin, norepinephrine into the blood. Only a few erythrocytes are involved in the formation of the aggregate in the amorphous type of sludge. The small size of the aggregates can represent no less, but even a greater danger to microcirculation, since their size allows them to penetrate into the smallest vessels up to and including the capillaries.

Sludge can also develop in case of poisoning with arsenic, cadmium, ether, chloroform, benzene, toluene, aniline. Sludge can be reversible or irreversible depending on the dose of the administered substance. Numerous clinical observations have found that changes in the protein composition of the blood can lead to the development of sludge. Conditions such as an increase in fibrinogen or a decrease in albumin, microglobulinemia increase blood viscosity and reduce its suspension stability.

Blood is a fluid that circulates in the circulatory system and carries gases and other dissolved substances necessary for metabolism or formed as a result of metabolic processes. Blood consists of plasma (a clear, pale yellow liquid) and cellular elements suspended in it. There are three main types of blood cells: red blood cells (erythrocytes), white blood cells (leukocytes), and platelets (platelets).

The red color of blood is determined by the presence of the red pigment hemoglobin in erythrocytes. In the arteries, through which the blood that has entered the heart from the lungs is transferred to the tissues of the body, hemoglobin is saturated with oxygen and is colored bright red; in the veins, through which blood flows from the tissues to the heart, hemoglobin is practically devoid of oxygen and darker in color.

Blood is a concentrated suspension of formed elements, mainly erythrocytes, leukocytes and platelets in plasma, and plasma, in turn, is a colloidal suspension of proteins, of which the most important for the problem under consideration are: serum albumin and globulin, as well as fibrinogen.

Blood is a rather viscous liquid, and its viscosity is determined by the content of red blood cells and dissolved proteins. Blood viscosity largely determines the rate at which blood flows through the arteries (semi-elastic structures) and blood pressure. The fluidity of blood is also determined by its density and the nature of the movement of various types of cells. Leukocytes, for example, move singly, in close proximity to the walls of blood vessels; erythrocytes can move both individually and in groups, like stacked coins, creating an axial, i.e. concentrating in the center of the vessel, flow.

The blood volume of an adult male is approximately 75 ml per kilogram of body weight; in an adult woman, this figure is approximately 66 ml. Accordingly, the total blood volume in an adult male is on average about 5 liters; more than half of the volume is plasma, with the remainder being mostly erythrocytes.

The rheological properties of blood have a significant impact on the amount of resistance to blood flow, especially in the peripheral circulatory system, which affects the work of the cardiovascular system, and, ultimately, the rate of metabolic processes in the tissues of athletes.

The rheological properties of blood play an important role in ensuring the transport and homeostatic functions of blood circulation, especially at the level of the microvascular bed. The viscosity of blood and plasma makes a significant contribution to vascular resistance to blood flow and affects the minute volume of blood. An increase in blood fluidity increases the oxygen transport capacity of the blood, which can play an important role in improving physical performance. On the other hand, hemorheological indicators can be markers of its level and overtraining syndrome.

Blood functions:

1. Transport function. Circulating through the vessels, the blood transports many compounds - among them gases, nutrients, etc.

2. Respiratory function. This function is to bind and transport oxygen and carbon dioxide.

3. Trophic (nutritional) function. Blood provides all cells of the body with nutrients: glucose, amino acids, fats, vitamins, minerals, water.

4. Excretory function. The blood carries away from the tissues the end products of metabolism: urea, uric acid and other substances removed from the body by excretion organs.

5. Thermoregulatory function. The blood cools the internal organs and transfers heat to the heat-transfer organs.

6. Maintaining the constancy of the internal environment. Blood maintains the stability of a number of body constants.

7. Ensuring water-salt exchange. Blood provides water-salt exchange between blood and tissues. In the arterial part of the capillaries, fluid and salts enter the tissues, and in the venous part of the capillary they return to the blood.

8. Protective function. Blood performs a protective function, being the most important factor in immunity, or protecting the body from living bodies and genetically alien substances.

9. Humoral regulation. Due to its transport function, blood provides chemical interaction between all parts of the body, i.e. humoral regulation. Blood carries hormones and other physiologically active substances.

Blood plasma is the liquid part of blood, a colloidal solution of proteins. It consists of water (90 - 92%) and organic and inorganic substances (8 - 10%). Of the inorganic substances in plasma, the most proteins (on average 7 - 8%) - albumins, globulins and fibrinogen ( fibrinogen-free plasma is called blood serum). In addition, it contains glucose, fat and fat-like substances, amino acids, urea, uric and lactic acid, enzymes, hormones, etc. Inorganic substances make up 0.9 - 1.0% of blood plasma. These are mainly salts of sodium, potassium, calcium, magnesium, etc. An aqueous solution of salts, which in concentration corresponds to the content of salts in the blood plasma, is called a physiological solution. It is used in medicine to replace missing body fluids.

Thus, the blood has all the functions of the tissue of the body - structure, special function, antigenic composition. But blood is a special tissue, liquid, constantly circulating throughout the body. Blood provides the function of supplying other tissues with oxygen and the transport of metabolic products, humoral regulation and immunity, coagulation and anticoagulation function. This is why blood is one of the most studied tissues in the body.

Studies of the rheological properties of the blood and plasma of athletes in the process of general aerocryotherapy showed a significant change in the viscosity of whole blood, hematocrit and hemoglobin. Athletes with low hematocrit, hemoglobin and viscosity have an increase, and athletes with a high hematocrit, hemoglobin and viscosity have a decrease, which characterizes the selective nature of the effect of OAKT, while there was no significant change in blood plasma viscosity.