Summary: Rheological properties of blood and their disorders in intensive care. Rheological properties of blood - what is it? Management of circulating blood volume, vascular tone and blood rheology

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 on different areas 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 in the areas of branching 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. Blood viscosity increases during 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 erythrocyte aggregation through depletion - the absence of high molecular weight proteins near erythrocytes, resulting in an "interaction pressure" similar in nature to osmotic pressure macromolecular solution, which brings the suspended particles closer together. 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.

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 on different areas vascular beds. 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 of the 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 more important factor, which 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 blood rheological 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.

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. From the structural organization of red membranes blood cells their aggregation activity and deformability, which are essential components in microcirculation. 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 works on blood hemorheology in patients with diabetes(SD) and metabolic syndrome(MS) 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.

Normal erythrocyte in normal conditions It has a biconcave disc 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 supports the diffusion of gases on high level throughout the microcirculation various bodies. 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 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 protein structures. 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 aregion. 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 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 prooxidant-antioxidant state, manifesting in different situations either antioxidant or prooxidant qualities.

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, a theory is widely accepted that considers membrane disorders as the leading causes of organ manifestations. various diseases, in particular in the pathogenesis of arterial hypertension in MS.

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, and a biological release reaction. 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. Max speed 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. Intravital 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 important place in cellular-humoral interaction of hemostasis systems. Literature data indicate a violation functional activity platelets are already early stage AG, 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 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 vessels associated with changes in blood rheology, transmural pressure and vasoconstrictor reactions in response to neurohumoral stimulation, then form morphological changes microcirculation vessels underlying 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 in 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 glycation of proteins, in particular erythrocytes, which is documented high content HbAc1, there are violations of the rheological parameters of the blood: a decrease in the 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 glycemic and lipid profiles of 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

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 thromboses

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 best method diagnosis and treatment.

1. Physical basis of hemorheology

IN normal conditions in almost all parts of the circulatory system, a laminar type of blood flow is observed. 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 stationary surface - 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 main arteries 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 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. That's why common property of such systems is their non-equilibrium. 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 sedimentation rate after they are added 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 blood with Ht 65% would turn into a dense homogeneous formation and blood flow would completely stop 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 with some hereditary diseases blood (sickle cell anemia), after operations in conditions of 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 departments 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. In this case, the viscosity of the plasma increases relative to normal level 2-3 times. IN clinical picture symptoms of severe microcirculation disorders begin to predominate: 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 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. Surgery or trauma is also accompanied by certain changes. cellular composition 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 associated shear rate factor must 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 speeds shift, 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 system of hemorheology in patients in critical condition, - transfer from high viscosity blood to low. This dynamic, however, is accompanied by a paradoxical deterioration in blood flow.

Hyperviscosity Syndrome. It is nonspecific and widespread in the clinic of internal diseases: in atherosclerosis, angina pectoris, chronic obstructive bronchitis, gastric ulcer, obesity, diabetes mellitus, endarteritis obliterans, 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 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 restoration 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 thrombi, 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 Ht that corresponds to safe level 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. A decrease in the 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 into 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. Similar effect possess epidural blockade, halogen-containing anesthetics, ganglionic blockers and nitrates. The rheological effect accompanies the main therapeutic effect these funds. The degree of decrease in blood viscosity is not predicted. It is defined current state 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 weight, 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 prophylactic and healing 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, peptic ulcer stomach, with 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 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 Dr. honey. 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

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 DO2 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.

Physical foundations 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 layer of the liquid can be considered motionless (Fig. 23.1). The viscosity of a simple fluid remains constant (8 s Poise), while 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.

Viscosity is due to the forces of inertia and cohesion.

Rice. 23.1. Viscosity as a proportionality factor between stress and shear rate.

Rice. 23.2. Dependence of relative blood viscosity (excluding shear rate) on hematocrit.

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

For a correct measurement and mathematical description of viscosity, concepts such as shear stress c and shear rate y are introduced. The first indicator is the ratio of the friction force between adjacent layers to their area - F/S. It is expressed in dynes/cm2 or pascals*. The second indicator is the layer velocity gradient - deltaV/L. It is measured in s-1.

According to Newton's equation, the shear stress is directly proportional to the shear rate: . 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.

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" (Fig. 23.2).

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.

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. A2- and beta-macroglobulins, fibrinogen degradation products, immunoglobulins act in a similar way. A closer approach of erythrocytes and their irreversible binding to each other is prevented by a negative membrane potential.

The main determinants of blood viscosity. Blood viscosity is influenced by many factors (Table 23.1). 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 (Fig. 23.3). 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" (rheological behavior) is generally accepted, emphasizing the "non-Newtonian" nature of blood fluidity.

Rice. 23.3. Relationship between DO2 and hematocrit.

Table 23.1.

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 blood with Ht 65% would turn into a dense homogeneous formation and blood flow would completely stop 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 section of the microcirculation. 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.

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.

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.

Methods for studying the rheological properties of blood. The "non-Newtonian" nature of blood and the associated shear rate factor must 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 measurement of blood viscosity in the CGS system is Poise (1 Poise = 10 dyn x s/cm2 = 0.1 Pa x s = 100 rel. units).

It is obligatory to measure blood viscosity in the range of low (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 et al. (1986) (Table 23.2).

Table 23.2.

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 nonspecific and widespread in the clinic of internal diseases: in atherosclerosis, angina pectoris, chronic obstructive bronchitis, gastric ulcer, obesity, diabetes mellitus, endarteritis obliterans, 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 in vitro hemoconcentration in such cases, blood hyperviscosity is detected.

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.

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 oppositely directed factors, DO2 to the tissues eventually develops. It can increase due to blood dilution or, conversely, significantly decrease under the influence of anemia.

The lowest Ht, which corresponds to a safe level of DO2, is called optimal. Its exact value is still the subject of debate. The quantitative ratios of Ht and DO2 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. A decrease in the 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.

Norvolemia hemodilution 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 into 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.

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 heparin fragments in a complex with antithrombin III inactivate thrombin, while heparin fragments with mol.m-7000 act mainly on activated factor X.

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.

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).