What is blood rheology? Open Library - open library of educational information Low blood viscosity syndrome
Hemorheology studies physicochemical characteristics blood, which determine its fluidity, i.e. the ability to undergo reversible deformation under the influence of external forces. A generally accepted quantitative measure of blood fluidity is its viscosity.
Deterioration in 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. During a hemodynamic crisis, blood viscosity also increases due to a decrease in blood flow velocity. A vicious circle arises that maintains stasis and shunting of blood in the microvasculature.
Disorders in the hemorheological system represent a universal mechanism for the pathogenesis of critical conditions, therefore optimization of the rheological properties of blood is the most important tool intensive care. Reducing blood viscosity helps accelerate blood flow, increase DO 2 to tissues, and facilitate heart function. With the help of rheologically active agents, it is possible to prevent the development of thrombotic, ischemic and infectious complications underlying disease.
Applied hemorheology is based on a number of physical principles of blood fluidity. Understanding them helps to choose the optimal method of diagnosis and treatment.
Physical foundations of hemorheology.
Under normal conditions in almost all departments circulatory system laminar type of blood flow is observed. It can be represented as an infinite number of layers of liquid 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. The adjacent layers still tend to move in the longitudinal direction, but the slower wall layers retard them. Inside the flow, friction occurs between the layers. A parabolic velocity distribution profile appears with a maximum in the center of the vessel. The near-wall layer of liquid can be considered stationary (Fig. 23.1). The viscosity of a simple fluid remains constant (8 cPoise), while the viscosity of blood varies depending on blood flow conditions (from 3 to 30 cPoise).
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 adhesion.
When the hematocrit is 0, the viscosity of the blood approaches the viscosity of plasma.
To correctly measure and mathematically describe 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/cm2 or pascals*. The second indicator is the velocity gradient of the layers - delta V/ L. It is measured in s -1.
In accordance with Newton's equation, shear stress is directly proportional to shear rate: . This means that the greater the speed difference between the layers of fluid, the greater their friction. And, conversely, equalizing the speed of fluid layers reduces mechanical stress along the watershed line. Viscosity in this case acts as a proportionality coefficient.
The viscosity of simple, or Newtonian, liquids (for example, water) is constant under any conditions of movement, i.e. There is a linear relationship between shear stress and shear rate for these fluids.
Unlike simple liquids, blood can change its viscosity when the speed of blood flow changes. Thus, 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 section of the microcirculation, despite the low shear stress, the viscosity increases 6-8 times relative to its level in the artery (i.e., up to 30-40 relative units). At extremely low, non-physiological shear rates, blood viscosity can increase 1000 times (!).
Thus, the relationship between shear stress and shear rate for whole blood is nonlinear, 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 elements and high-molecular substances) is suspended. The dispersed phase particles are large enough to resist Brownian motion. Therefore, a common property of such systems is their nonequilibrium. The components of the dispersed phase constantly strive to separate and precipitate cellular aggregates from the dispersed medium.
Basic and rheologically most meaningful view blood cellular aggregates - erythrocyte. It is a multidimensional cellular complex with typical form"coin column" 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 initially increased speed sedimentation after their addition to single-group plasma healthy person begin to settle at normal speed. And vice versa, if the red blood cells of a healthy person with a normal sedimentation rate are placed in the plasma of a patient, then their precipitation will significantly accelerate.
Natural inducers of aggregation include primarily fibrinogen. The length of its molecule is 17 times greater than its width. Thanks 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 influence of minimal mechanical force. They act in a similar way A 2 - and beta-macroglobulins, fibrinogen degradation products, immunoglobulins. A negative membrane potential prevents closer proximity of red blood cells and their irreversible binding to each other.
It should be emphasized that erythrocyte aggregation is a normal rather than pathological process. Its positive side is that it facilitates the passage of blood through the microcirculation system. When aggregates form, the surface to volume ratio decreases. As a result, the frictional resistance of the unit turns out to be significantly less than the resistance of its individual components.
Main determinants of blood viscosity.
Blood viscosity is influenced by many factors (Table 23.1). All of them realize their effect by changing the viscosity of plasma or the rheological properties of blood cells.
The erythrocyte is the main cellular 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). Thus, when Ht increases from 30 to 60%, the relative viscosity of blood doubles, and when Ht increases from 30 to 70%, it triples. Hemodilution, on the contrary, reduces blood viscosity.
The term “rheological behavior of blood” is generally accepted and emphasizes the “non-Newtonian” nature of blood fluidity.
Deformability of erythrocytes.
The diameter of the red blood cell 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 were not capable of deformation, then blood with Ht 65% would turn into a dense homogeneous formation and a complete stop of blood flow would occur in the peripheral parts of the circulatory system. However, due to the ability of red blood cells 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 general principles transition of sol to 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 certain hereditary diseases blood (sickle cell anemia), after operations under artificial circulation. At the same time, the shape of red blood cells and their plasticity change. Increased blood viscosity is observed, which does not correspond to low Ht.
Plasma viscosity.
Plasma as a whole can be classified as a “Newtonian” fluid. 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. However, plasma has a very significant effect on peripheral blood flow. In capillaries, blood viscosity is reduced by half compared to proximal and distal vessels of larger diameter (phenomenon §). This “prolapse” of viscosity is associated with the axial orientation of red blood cells 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”, which ensures the sliding of the chain of blood cells with minimal friction.
This mechanism functions only when the plasma protein composition is normal. An increase in the level of fibrinogen or any other globulin leads to difficulty in capillary blood flow, sometimes of a critical nature. Thus, multiple myeloma, Waldenström's macroglobulinemia and some collagenoses are accompanied by excessive production of immunoglobulins. In this case, the plasma viscosity increases relative to normal level 2-3 times. The clinical picture begins to be dominated by symptoms of severe microcirculation disorders: decreased vision and hearing, drowsiness, adynamia, headache, paresthesia, bleeding of mucous membranes.
Pathogenesis of hemorheological disorders. In intensive care practice, hemorheological disorders arise 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, fibrinogen levels usually double. The peak of this increase occurs on days 3-5, and normalization of fibrinogen levels occurs only at 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 quantities. 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 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 during uncomplicated abdominal interventions, the volumetric velocity of blood flow 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 surgery. 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 disrupted, and microcirculatory stasis occurs.
Hemorheological disorders and venous thrombosis.
Slowing down the speed of movement in the venous circulation provokes aggregation of red blood cells. However, the inertia of movement may be quite large and the blood cells will experience increased deformation load. Under its influence, ATP is released from red blood cells - a powerful inducer of platelet aggregation. Low speed shear also stimulates the adhesion of young granulocytes to the wall of venules (Farheus-Vejiens phenomenon). Irreversible aggregates are formed that can form the cellular core of a venous thrombus.
Further development of the situation will depend on the activity of fibrinolysis. As a rule, between the processes of formation and resorption of a blood clot, a unstable equilibrium. For this reason, most cases of deep vein thrombosis lower limbs in hospital practice, it occurs latently and resolves spontaneously, without consequences. The use of disaggregants and anticoagulants is a highly effective way to prevent venous thrombosis.
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 a stator and a rotor congruent with it. The gap between them serves as a working chamber and is filled with a blood sample. The movement of the liquid is initiated by the rotation of the rotor. This, in turn, is arbitrarily specified in the form of a certain shear rate. The measured quantity is the shear stress, which occurs as a mechanical or electrical torque necessary to maintain the selected speed. Blood viscosity is then calculated using Newton's formula. The unit of measurement for blood viscosity in the GHS system is Poise (1 Poise = 10 dyne x s/cm 2 = 0.1 Pa x s = 100 relative units).
It is mandatory to measure blood viscosity in the low range (<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 red blood cells to aggregate. High shear rates (200-400 s -1) are achieved in vivo in the aorta, great vessels and capillaries. In this case, as rheoscopic observations show, red blood cells occupy a predominantly axial position. They stretch in the direction of movement, their membrane begins to rotate relative to the cellular contents. Due to hydrodynamic forces, almost complete disaggregation of blood cells is achieved. Viscosity, determined at high shear rates, depends primarily on the plasticity of the red blood cells and the shape of the cells. It is called dynamic.
As a standard for research on a rotational viscometer and the corresponding norm, you can use the indicators according to the method of N.P. Alexandrova et al. (1986)
To provide a more detailed picture of the rheological properties of blood, several more specific tests are performed. The deformability of erythrocytes is assessed by the speed 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 measuring the change in the optical density of the medium after adding aggregation inducers (ADP, serotonin, thrombin or adrenaline) to it.
Diagnosis of hemorheological disorders .
Disorders in the hemorheological system, as a rule, occur latently. Their clinical manifestations are nonspecific and subtle. Therefore, the diagnosis is determined mainly by laboratory data. Its leading criterion is the value of blood viscosity.
The main direction of shifts in the hemorheology system in patients in critical condition is the transition from increased to decreased blood viscosity. This dynamics, however, is accompanied by a paradoxical deterioration in blood fluidity.
Syndrome of increased blood viscosity.
It is nonspecific in nature and is widespread in the clinic of internal diseases: with atherosclerosis, angina pectoris, chronic obstructive bronchitis, gastric ulcer, obesity, diabetes mellitus, obliterating endarteritis etc. At the same time, a moderate increase in blood viscosity is noted up to 35 cPoise at y = 0.6 s -1 and 4.5 cPoise 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 an underlying condition.
Low blood viscosity syndrome.
As the critical condition unfolds, blood viscosity decreases due to hemodilution. Viscometry indicators are 20-25 cPoise at y=0.6 s -1 and 3-3.5 cPoise 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 - to 2.5-2.8 cPoise and structural blood viscosity - to 15-18 cPoise.
The low value of blood viscosity in a patient in critical condition creates a misleading impression of hemorheological well-being. Despite hemodilution, with low blood viscosity syndrome, microcirculation significantly deteriorates. The aggregation activity of red blood cells increases 2-3 times, and the passage of the erythrocyte suspension through nucleopore filters slows down 2-3 times. After restoration of Ht by hemoconcentration in vitro, blood hyperviscosity is found in such cases.
Against the background of low or very low blood viscosity, massive aggregation of red blood cells can 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 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 caused by other, non-rheological mechanisms.
Clinical manifestations of low blood viscosity syndrome:
- tissue hypoxia (in the absence of hypoxemia);
- increased peripheral vascular resistance;
- deep vein thrombosis of the extremities, recurrent pulmonary thromboembolism;
- adynamia, stupor;
- deposition of blood in the liver, spleen, subcutaneous vessels.
Prevention and treatment. Patients admitted to the operating room or intensive care unit need to optimize the rheological properties of blood. This prevents the formation of venous blood clots, reduces the likelihood of ischemic and infectious complications, and alleviates the course of the underlying disease. Most effective techniques rheological therapy is the dilution of blood and suppression of the aggregation activity of its formed elements.
Hemodilution.
The red blood cell is the main carrier of structural and dynamic resistance to blood flow. Therefore, hemodilution turns out to be the most effective rheological agent. Its beneficial effect has been known for a long time. For many centuries, bloodletting was perhaps the most common method of treating diseases. The appearance of low molecular weight dextrans was the next stage 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 differently directed factors, DO 2 ultimately develops in the tissues. It can increase due to blood dilution or, on the contrary, 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 size is still a matter of debate. The quantitative relationships between Ht and DO 2 are well known. However, it is not possible to assess the contribution of individual factors: tolerance of anemia, tension of tissue metabolism, hemodynamic reserve, etc. According to the general opinion, the goal of therapeutic hemodilution is Ht 30-35%. However, experience in treating massive blood loss without blood transfusion shows that an even greater reduction in Ht to 25 and even 20% is quite safe from the point of view of oxygen supply to tissues.
Currently, three techniques are used to achieve hemodilution.
Hemodilution in hypervolemic mode
implies a fluid transfusion that leads to a significant increase in blood volume. In some cases, a short-term infusion of 1-1.5 liters of plasma substitutes precedes induction of anesthesia and surgical intervention, in other cases requiring longer hemodilution, a decrease in Ht is achieved with 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 normovolemic mode
was originally proposed as an alternative to heterologous transfusions in surgery. The essence of the method is the preoperative collection 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 a rate of 1:2. With some modification of the method, it is possible to collect 2-3 liters of autologous blood without any adverse hemodynamic and hematological consequences. Collected blood then returned during or after surgery.
Normovolemic hemodilution is not only a safe, but also a 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 postoperative complications. This method can be widely used for planned surgical interventions.
Endogenous hemodilution
develops with pharmacological vasoplegia. The decrease in Ht in these cases is due to the fact that 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 these funds. The degree of reduction 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 (cattle lungs). The final product is a mixture of polysaccharide fragments with different molecular weights, but with similar biological activity.
The largest heparin fragments in complex with antithrombin III inactivate thrombin, while heparin fragments with a molecular weight of 7000 act predominantly on the activated factor X.
The administration of high molecular weight heparin in a dose of 2500-5000 units subcutaneously 4-6 times a day in the early postoperative period has become a widespread practice. Such a prescription reduces the risk of thrombosis and thromboembolism by 1.5-2 times. Low 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 collateral), are the main and most effective methods for the prevention of hemorheological disorders in surgical patients.
Low molecular weight fractions of heparin have less affinity for platelet von Willebrand factor. Because of this, compared to high molecular weight heparin, they are even less likely to cause thrombocytopenia and bleeding. The first experience of using low molecular weight heparin (Clexane, Fraxiparin) in clinical practice gave encouraging results. Heparin preparations turned out to be equipotential to traditional heparin therapy, and according to some data even exceeded its preventive and healing effect. In addition to safety, low-molecular-weight heparin fractions are also distinguished by their economical administration (once daily) and the absence of the need for aPTT monitoring. The dose selection is usually made without taking into account body weight.
Plasmapheresis.
The traditional rheological indication for plasmapheresis is primary hyperviscosity syndrome, which is caused by excessive production of abnormal proteins (paraproteins). Their removal leads to rapid reversal of the disease. The effect, however, is short-lived. The procedure is symptomatic.
Currently, plasmapheresis is actively used for preoperative preparation 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. Replace up to 1/2 of the volume of the central processing unit.
The decrease in globulin levels and plasma viscosity after one plasmapheresis procedure can be significant, but short-lived. The main beneficial effect of the procedure, which applies to the entire postoperative period, is the so-called resuspension phenomenon. Washing of erythrocytes in a protein-free environment 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 irradiation of blood with a helium-neon laser (wavelength 623 nm) of low power (2.5 mW), a clear and long-lasting 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 is normalized. Blood viscosity 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 assumed 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).
Ultraviolet irradiation of colloidal preparations (for example, rheopolyglucin) has also been proposed. After their administration, the dynamic and structural viscosity of blood decreases by 1.5 times. Platelet aggregation is also significantly inhibited. It is characteristic that unmodified rheopolyglucin is not able to reproduce all these effects.
Moves at different speeds, which depend on the contractility of the heart, functional state bloodstream. At a relatively low flow rate, blood particles are located parallel to each other. This flow is laminar, while the blood flow is layered. If the linear speed of blood increases and becomes greater than a certain value, its flow becomes erratic (the so-called “turbulent” flow).
The speed of blood flow is determined using the Reynolds number; its value at which laminar flow becomes turbulent is approximately 1160. Data indicate that turbulence of blood flow is possible in the large branches and at the beginning of the aorta. Most vessels are characterized by laminar blood flow. The movement of blood through the vessels is also determined by other important parameters: “shear stress” and “shear rate”.
Blood viscosity will depend on the shear rate (range 0.1-120 s-1). If the shear rate is greater than 100 s-1, changes in blood viscosity are not clearly expressed; after the shear rate reaches 200 s-1, the viscosity does not change.
Shear stress is the force acting on a unit surface area of a container and is measured in pascals (Pa). Shear rate is measured in reciprocal seconds (s-1), this parameter indicates the speed at which layers of fluid moving in parallel move relative to each other. Blood is characterized by its viscosity value. It is measured in pascal seconds and is defined as the ratio of shear stress to shear rate.
How are blood properties assessed?
The main factor influencing blood viscosity is the concentration of red blood cells, which is called hematocrit. Hematocrit is determined from a blood sample using centrifugation. Blood viscosity also depends on temperature and is also determined by the composition of proteins. Fibrinogen and globulins have the greatest influence on blood viscosity.
The task of developing rheology analysis methods that would objectively reflect the properties of blood still remains relevant.
Of main importance for assessing the properties of blood is its aggregation state. The main methods for measuring blood properties are carried out using viscometers various types: instruments are used that operate according to the Stokes method, as well as on the principle of recording electrical, mechanical, and acoustic vibrations; rotational rheometers, capillary viscometers. The use of rheological technology makes it possible to study the biochemical and biophysical properties of blood in order to control microregulation in metabolic and hemodynamic disorders.
Currently, the problem of microcirculation attracts much attention from theorists and clinicians. Unfortunately, the accumulated knowledge in this area has not yet received proper application in the practical activities of a doctor due to the lack of reliable and available methods diagnostics However, without understanding the basic laws of tissue circulation and metabolism, it is impossible to correctly use modern means infusion therapy.
The microcirculation system plays an extremely important role in providing tissues with blood. This occurs mainly due to the vasomotion reaction, which is carried out by vasodilators and vasoconstrictors in response to changes in tissue metabolism. Capillary network makes up 90% of the circulatory system, but 60-80% of it remains inactive.
The microcirculatory system forms a closed blood flow between arteries and veins (Fig. 3). It consists of arterpoles (diameter 30-40 µm), which end in terminal arterioles (20-30 µm), which are divided into many metarterioles and precapillaries (20-30 µm). Further, at an angle close to 90°, rigid tubes devoid of a muscular membrane diverge, i.e. true capillaries (2-10 µm).
Rice. 3. A simplified diagram of the distribution of vessels in the microcirculatory system 1 - artery; 2 - terminal artery; 3 - arterrol; 4 - terminal arteriole; 5 - metarteril; 6 - precapillary with muscle sphincter (sphincter); 7 - capillary; 8 - collecting venule; 9 - venule; 10 - vein; 11 - main channel (central trunk); 12 - arteriolo-venular shunt.
Metarterioles at the level of precapillaries have muscle sphincter that regulates the flow of blood into the capillary bed and at the same time creates what is necessary for the functioning of the heart peripheral resistance. Precapillaries are the main regulatory element of microcirculation, ensuring the normal function of macrocirculation and transcapillary exchange. The role of precapillaries as regulators of microcirculation is especially important in various violations volemia, when the level of bcc depends on the state of transcapillary exchange.
The continuation of the metarterioles forms the main canal (central trunk), which passes into the venous system. The collecting veins, which extend from the venous section of the capillaries, also flow here. They form prevenules, which have muscular elements and are capable of blocking the flow of blood from the capillaries. Prevenules collect into venules and form a vein.
There is a bridge between arterioles and venules - an arteriole-venous shunt, which is actively involved in the regulation of blood flow through microvessels.
Blood flow structure. Blood flow in the microcirculation system has a certain structure, which is determined primarily by the speed of blood movement. In the center of the blood flow, creating an axial line, there are red blood cells, which, together with the plasma, move one after another at a certain interval. This flow of red blood cells creates an axis around which other cells - white blood cells and platelets - are located. The erythrocyte current has the highest rate of advancement. Platelets and leukocytes located along the vessel wall move more slowly. The location of the components of the blood is quite specific and does not change at normal blood flow speed.
Directly in the true capillaries, the blood flow is different, since the diameter of the capillaries (2-10 microns) is less than the diameter of the red blood cells (7-8 microns). In these vessels, the entire lumen is occupied mainly by red blood cells, which acquire an elongated configuration in accordance with the lumen of the capillary. The wall layer of plasma is preserved. It is necessary as a lubricant for the gliding of red blood cells. Plasma also retains the electrical potential of the erythrocyte membrane and its biochemical properties, on which the elasticity of the membrane itself depends. In the capillary, the blood flow is laminar, its speed is very low - 0.01-0.04 cm/s at a blood pressure of 2-4 kPa (15-30 mm Hg).
Rheological properties blood. Rheology is the science of fluidity of liquid media. She studies mainly laminar flows, which depend on the relationship between inertial and viscosity forces.
Water has the lowest viscosity, allowing it to flow in any conditions, regardless of flow speed and temperature. Non-Newtonian fluids, which include blood, do not obey these laws. The viscosity of water is a constant value. Blood viscosity depends on a number of physicochemical parameters and varies widely.
Depending on the diameter of the vessel, the viscosity and fluidity of the blood change. The Reynolds number reflects the inverse relationship between the viscosity of the medium and its fluidity, taking into account the linear forces of inertia and the diameter of the vessel. Microvessels with a diameter of no more than 30-35 microns have positive influence the viscosity of the blood flowing in them and its fluidity increases as it penetrates into narrower capillaries. This is especially pronounced in capillaries with a diameter of 7-8 microns. However, in smaller capillaries the viscosity increases.
Blood is in constant movement. This is its main characteristic, its function. As blood flow speed increases, blood viscosity decreases and, conversely, as blood flow slows down, it increases. However, there is also inverse relationship: The speed of blood flow is determined by viscosity. To understand this purely rheological effect, one must consider the blood viscosity index, which is the ratio of shear stress to shear rate.
The blood flow consists of layers of fluid that move in parallel, and each of them is under the influence of a force that determines the shear (“shear stress”) of one layer in relation to the other. This force is created by the systolic arterial pressure.
The viscosity of blood is influenced to a certain extent by the concentration of the ingredients it contains - red blood cells, nuclear cells, proteins, fatty acids, etc.
Red blood cells have an internal viscosity, which is determined by the viscosity of the hemoglobin they contain. The internal viscosity of an erythrocyte can vary within wide limits, which determines its ability to penetrate narrower capillaries and take on an elongated shape (thixitropia). Basically, these properties of the erythrocyte are determined by the content of phosphorus fractions in it, in particular ATP. Hemolysis of erythrocytes with the release of hemoglobin into plasma increases the viscosity of the latter by 3 times.
Proteins are extremely important for characterizing blood viscosity. A direct dependence of blood viscosity on the concentration of blood proteins has been revealed, especially A 1 -, A 2-, beta- and gamma-globulins, as well as fibrinogen. Albumin plays a rheologically active role.
Other factors that actively influence blood viscosity include fatty acid, carbon dioxide. Normal blood viscosity averages 4-5 cP (centipoise).
Blood viscosity, as a rule, is increased during shock (traumatic, hemorrhagic, burn, toxic, cardiogenic, etc.), dehydration, erythrocythemia and a number of other diseases. In all these conditions, microcirculation is primarily affected.
To determine viscosity, there are capillary-type viscometers (Oswald designs). However, they do not meet the requirement of determining the viscosity of moving blood. In this regard, viscometers are currently being designed and used, which are two cylinders of different diameters rotating on the same axis; blood circulates in the gap between them. The viscosity of such blood should reflect the viscosity of the blood circulating in the vessels of the patient’s body.
The most severe disturbance of the structure of capillary blood flow, fluidity and viscosity of blood occurs due to aggregation of erythrocytes, i.e. gluing red cells together to form “coin columns” [Chizhevsky A.L., 1959]. This process is not accompanied by hemolysis of red blood cells, as with agglutination of an immunobiological nature.
The mechanism of erythrocyte aggregation may be associated with plasma, erythrocyte or hemodynamic factors.
Among the plasma factors, the main role is played by proteins, especially those with high molecular weight, which violate the ratio of albumin and globulins. A 1 - and a 2 - and beta-globulin fractions, as well as fibrinogen, have a high aggregation ability.
Violations of the properties of erythrocytes include changes in their volume, internal viscosity with loss of membrane elasticity and ability to penetrate the capillary bed, etc.
A slowdown in blood flow is often associated with a decrease in shear rate, i.e. occurs when blood pressure drops. Aggregation of erythrocytes is observed, as a rule, with all types of shock and intoxication, as well as with massive blood transfusions and inadequate artificial circulation [Rudaev Ya.A. et al., 1972; Soloviev G.M. et al., 1973; Gelin L. E., 1963, etc.].
Generalized aggregation of erythrocytes is manifested by the “sludge” phenomenon. The name for this phenomenon was proposed by M.N. Knisely, “sludging”, in English “swamp”, “mud”. Aggregates of erythrocytes undergo resorption in the reticuloendothelial system. This phenomenon always causes a difficult prognosis. Necessary prompt application disaggregation therapy using low molecular weight solutions of dextran or albumin.
The development of “sludge” in patients can be accompanied by a very deceptive pinking (or redness) of the skin due to the accumulation of sequestered red blood cells in non-functioning subcutaneous capillaries. This clinical picture of “sludge”, i.e. the last stage of development of erythrocyte aggregation and disruption of capillary blood flow is described by L.E. Gelin in 1963 under the name “red shock”. The patient’s condition is extremely serious and even hopeless if sufficiently intensive measures are not taken.
Occurring during inflammatory processes in the lungs changes at the cellular and subcellular levels have a significant impact on the rheological properties of blood, and through impaired metabolism of biologically active substances (BAS) and hormones - on the regulation of local and systemic blood flow. As is known, the state of the microcirculatory system is largely determined by its intravascular component, studied by hemorheology. Such manifestations of hemorheological properties of blood, such as the viscosity of plasma and whole blood, patterns of fluidity and deformation of its plasma and cellular components, the process of blood clotting - all this can clearly respond to many pathological processes in the body, including the process of inflammation.
Development of inflammatory process in lung tissue is accompanied by a change in the rheological properties of blood, increased aggregation of erythrocytes, leading to microcirculation disorders, the occurrence of stasis and microthrombosis. There was a positive correlation between changes in the rheological properties of blood and the severity of inflammatory process and the degree of intoxication syndrome.
Evaluating blood viscosity state in patients with various forms COPD, most researchers found it enlarged. In some cases, in response to arterial hypoxemia, polycythemia occurs in patients with COPD with an increase in hematocrit to 70%, which significantly increases blood viscosity, allowing some researchers to classify this factor as one that increases pulmonary vascular resistance and the load on the right side of the heart. The combination of these changes in COPD, especially with exacerbation of the disease, causes a deterioration in the properties of blood fluidity and the development of a pathological syndrome of increased viscosity. At the same time, increased viscosity blood in these patients can be observed with normal hematocrit and plasma viscosity.
Of particular importance for rheological state of blood have aggregation properties of erythrocytes. Almost all studies that studied this indicator in patients with COPD indicate an increased ability to aggregate erythrocytes. Moreover, there was often a close connection between an increase in blood viscosity and the ability of red blood cells to aggregate. During the process of inflammation in patients with COPD, the amount of coarse, positively charged proteins (fibrinogen, C-reactive protein, globulins) sharply increases in the bloodstream, which, combined with a decrease in the number of negatively charged albumins, causes a change in the hemoelectric status of the blood. Adsorbed on the erythrocyte membrane, positively charged particles cause a decrease in its negative charge and suspension stability of the blood.
For red blood cell aggregation immunoglobulins of all classes, immune complexes and complement components are influenced, which can play a significant role in patients bronchial asthma(BA).
Red blood cells determine the rheology of blood and another property - deformability, i.e. the ability to undergo significant changes in shape when interacting with each other and with the lumen of the capillaries. A decrease in the deformability of erythrocytes, together with their aggregation, can lead to blocking of individual areas in the microcirculation system. It is believed that this ability of erythrocytes depends on the elasticity of the membrane, the internal viscosity of the cell contents, and the ratio of the cell surface to their volume.
In patients with COPD, including those with BA, almost all researchers found a decrease red blood cell abilities to deformation. Hypoxia, acidosis and polyglobulia are considered to be the causes of increased rigidity of erythrocyte membranes. With the development of a chronic inflammatory bronchopulmonary process, functional failure progresses, and then severe morphological changes erythrocytes, which are manifested by a deterioration in their deformation properties. Due to an increase in the rigidity of erythrocytes and the formation of irreversible erythrocyte aggregates, the “critical” radius of microvascular patency increases, which contributes to a sharp disruption of tissue metabolism.
The role of aggregation platelets in hemorheology is of interest, first of all, due to its irreversibility (in contrast to erythrocyte) and the active participation in the process of platelet adhesion of a number of biologically active substances (BAS), which are essential for changes in vascular tone and the formation of bronchospastic syndrome. Platelet aggregates also have a direct capillary-blocking effect, forming microthrombi and microemboli.
During the progression of COLD and the formation of CHL, functional failure develops blood platelets, which is characterized by an increase in the aggregation and adhesive ability of platelets against the background of a decrease in their disaggregation properties. As a result of irreversible aggregation and adhesion, “viscous metamorphosis” of platelets occurs; various biologically active substrates are released into the microcirculatory bed, which serves as a trigger for the process of chronic intravascular microcoagulation, which is characterized by a significant increase in the intensity of the formation of fibrin and platelet aggregates. It has been established that disturbances in the hemocoagulation system in patients with COPD can cause additional disorders of the pulmonary microcirculation, including recurrent thromboembolism of small vessels of the lung.
T.A. Zhuravleva revealed a clear dependence of the severity microcirculation disorders and rheological properties of blood from the active inflammatory process during acute pneumonia with the development of hyper-coagulation syndrome. Violations of the rheological properties of blood were especially pronounced in the phase of bacterial aggression and gradually disappeared as the inflammatory process was eliminated.
In asthma there is active inflammation leads to significant disturbances in the rheological properties of blood and, in particular, to an increase in its viscosity. This is realized by increasing the strength of erythrocyte and platelet aggregates (which is explained by the influence of a high concentration of fibrinogen and its degradation products on the process of aggregation), an increase in hematocrit, and changes in the protein composition of plasma (an increase in the concentration of fibrinogen and other coarse proteins).
Our studies of asthma patients showed that this pathology is characterized by a decrease in the rheological properties of blood, which are corrected under the influence of trental. When comparing the rheological properties of patients in the mixed venous (at the entrance to the ICC) and in arterial blood(at the exit from the lungs) it was found that during circulation in the lungs there is an increase in the fluidity properties of blood. Patients with asthma who have concomitant systemic arterial hypertension, was characterized by a reduced ability of the lungs to improve the deformability properties of red blood cells.
In the process of correction rheological disturbances in the treatment of asthma with trental, a high degree of correlation was noted between an improvement in pulmonary function indicators and a decrease in diffuse and local changes in pulmonary microcirculation, determined using perfusion scintigraphy.
Inflammatory lung tissue damage in COPD, they cause disturbances in its metabolic functions, which not only directly affect the state of microhemodynamics, but also cause pronounced changes in hematohistological metabolism. In patients with COPD, a direct relationship was revealed between an increase in the permeability of capillary-connective tissue structures and an increase in the concentration of histamine and serotonin in the bloodstream. These patients have disturbances in the metabolism of lipids, glucocorticoids, kinins, and prostaglandins, which leads to disruption of the mechanisms of cellular and tissue adaptation, changes in microvascular permeability and the development of capillary-trophic disorders. Morphologically, these changes are manifested by perivascular edema, pinpoint hemorrhages and neurodystrophic processes with damage to the perivascular connective tissue and lung parenchyma cells.
As rightly noted by L.K. Surkov and G.V. Egorova, in patients chronic inflammatory diseases respiratory organs, disruption of hemodynamic and metabolic homeostasis as a result of significant immunocomplex damage to the vessels of the microvasculature of the lungs negatively affects the overall dynamics of tissue inflammatory reaction and is one of the mechanisms of chronicization and progression of the pathological process.
Thus, the existence of close relationships between microcirculatory blood flow in tissues and the metabolism of these tissues, as well as the nature of these changes during inflammation in patients with COPD, indicate that not only the inflammatory process in the lungs causes changes in microvascular blood flow, but also, for its part, a violation of microcirculation leads to an aggravation of the inflammatory process, those. a vicious circle arises.
Blood is a fluid that circulates in the circulatory system and carries gases and other dissolved substances necessary for metabolism or resulting from metabolic processes. Blood consists of plasma ( clear liquid pale yellow) 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 red blood cells. In the arteries, through which blood entering the heart from the lungs is transported to the tissues of the body, hemoglobin is saturated with oxygen and colored bright red; in the veins through which blood flows from tissues to the heart, hemoglobin is practically devoid of oxygen and is 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 greatly influences the speed at which blood flows through arteries (semi-elastic structures) and blood pressure. The fluidity of blood is also determined by its density and the pattern of movement of various types of cells. White blood cells, for example, move singly, in close proximity to the walls of blood vessels; red blood cells can move either individually or in groups like stacked coins, creating an axial, i.e. concentrating in the center of the vessel, flow.
An adult male's blood volume is approximately 75 ml per kilogram of body weight; at adult woman this figure is approximately 66 ml. Accordingly, the total blood volume in an adult man is on average about 5 liters; more than half the volume is plasma, with the remainder being mainly red blood cells.
The rheological properties of blood have a significant impact on the resistance to blood flow, especially in the peripheral circulatory system, which affects the work of cardio-vascular system, and, ultimately, on the speed of metabolic processes in the tissues of athletes.
The rheological properties of blood play important role in ensuring 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 minute blood volume. Increasing blood fluidity increases the oxygen transport capacity of the blood, which can play an important role in increasing 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, 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. Blood carries away metabolic end products from tissues: urea, uric acid and other substances removed from the body by excretory organs.
5. Thermoregulatory function. Blood cools internal organs and transfers heat to the heat transfer organs.
6. Maintaining consistency internal environment. Blood maintains the stability of a number of body constants.
7. Ensuring water-salt metabolism. Blood ensures 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 protective function, being the most important factor immunity, or the body’s defense against living bodies and genetically foreign substances.
9. Humoral regulation. Thanks to its transport function, blood ensures chemical interaction between all parts of the body, i.e. humoral regulation. Blood carries hormones and other physiological active substances.
Blood plasma is the liquid part of blood, a colloidal solution of proteins. Its composition includes water (90 - 92%) and organic and inorganic substances (8 - 10%). Of the inorganic substances in plasma, the most proteins (on average 7 - 8%) are albumins, globulins and fibrinogen. ( plasma that does not contain fibrinogen 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. Water solution salts, which in concentration corresponds to the content of salts in the blood plasma, is called saline solution. It is used in medicine to replenish missing fluids in the body.
Thus, blood has all the functions of body tissue - 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 transporting metabolic products, humoral regulation and immunity, coagulation and anticoagulation functions. This is why blood is one of the most studied tissues in the body.
Studies of the rheological properties of blood and plasma of athletes during general aerocryotherapy showed a significant change in the viscosity of whole blood, hematocrit and hemoglobin. Athletes with low values of hematocrit, hemoglobin and viscosity have an increase, and athletes with high rate hematocrit, hemoglobin and viscosity - a decrease, which characterizes the selective nature of the effects of OACT; however, no significant change in blood plasma viscosity was observed.