Violation of the microcirculation of blood vessels. Intravascular mechanisms of microcirculation disorders

admitted
All-Russian educational and methodological center
for Continuing Medical and Pharmaceutical Education
Ministry of Health of the Russian Federation
as a textbook for medical students

10.1. Structural and functional aspects and physiology of microcirculation

Links of the cardiovascular system		Function
1st link	Heart and great vessels (arteries)	pump and smoothing of pulsation (in the heart, blood pressure drops from 150 to 0, and in large arteries from 120 to 80 mm Hg)
2nd link	Arterioles	resistant vessels and (resistance to blood flow)
	precapillary sphincters	regulation of blood flow through the organ, regulation of blood pressure
	Arterio-venular shunts	shunting of blood around the capillaries (from arterioles to venules) - inefficient blood flow
3rd link	capillaries	exchange of blood and cells with gases and nutrients. Blood flow and blood pressure are constant
4th link	Venules, veins	capacitive vessels, contain up to 70-80% of all blood. Low BP, slow blood flow

The microcirculatory link is the key one. The work of the heart and all parts of the cardiovascular system is adapted to create optimal conditions for microcirculation (low and constant blood pressure, blood flow is provided with the best conditions for the entry of metabolic products, fluid into the bloodstream from cells and vice versa).

Arterioles are afferent vessels. Inner diameter - 40 nm, metarterioles - 20 nm, precapillary sphincters - 10 nm. All are characterized by the presence of a pronounced muscular membrane, therefore they are called resistive vessels. The precapillary sphincter is located at the point of departure from the metarteriole of the precapillary. As a result of contraction and relaxation of the precapillary sphincter, regulation of the blood supply to the bed following the precapillary is achieved.
Capillaries are exchange vessels. This component of the microcirculation channel includes capillaries, in some organs they are called sinusoids because of their peculiar shape and function (liver, spleen, bone marrow). According to modern concepts, a capillary is a thin tube with a diameter of 2-20 nm, formed by a single layer of endothelial cells, without muscle cells. Capillaries branch off from arterioles, they can expand and narrow, i.e. change its diameter regardless of the reaction of arterioles. The number of capillaries is approximately 40 billion, the total length is 800 km, the area is 1000 m 2, each cell is removed from the capillary by no more than 50-100 nm.
Venules are efferent vessels with a diameter of about 30 nm. There are far fewer muscle cells in the walls compared to arterioles. Features of hemodynamics in the venous section are due to the presence in venules with a diameter of 50 nm or more, valves that prevent reverse blood flow. The thinness of the venules and veins, their large number (2 times more than the afferent vessels) creates huge prerequisites for the deposition and redistribution of blood from the resistive channel to the capacitive one.
Vascular bridges - "bypass channels" between arterioles and venules. Found in almost all parts of the body. Since these formations occur exclusively at the level of the microcirculatory bed, it is more correct to call them "arteriolo-venular anastomoses", their diameter is 20-35 nm, from 25 to 55 anastomoses are recorded on a tissue with an area of 1.6 cm 2.

Physiology of microcirculation. The main function is the transcapillary exchange of gases and chemicals. Depends on the following factors:

Velocity of blood flow in the microvasculature. The linear velocity of blood flow in the aorta and large human arteries is 400-800 mm/sec. In the channel, it is much less: in arterioles - 1.5 mm/sec; in capillaries - 0.5 mm/sec; in large veins - 300 mm / sec. Thus, the linear velocity of blood flow progressively decreases from the aorta to the capillaries (due to an increase in the cross-sectional area of the bloodstream and a decrease in blood pressure), then the blood flow velocity increases again in the direction of blood flow to the heart.
Blood pressure in the microcirculation. Since the linear velocity of blood flow is directly proportional to blood pressure, as the branching of the bloodstream from the heart to the capillaries, blood pressure decreases. In large arteries, it is 150 mm Hg, in the microcirculation - 30 mm Hg, in the venous section - 10 mm Hg.
Vasomotion is a reaction of spontaneous narrowing and expansion of the lumen of metarterioles and precapillary sphincters. Phases - from several seconds to several minutes. They are determined by changes in the content of tissue hormones: histamine, serotonin, acetylcholine, kinins, leukotrienes, prostaglandins.
capillary permeability. The focus is on the problem of permeability of capillary wall biomembranes. The forces of the transition of substances and gases through the capillary wall are:
- diffusion - mutual penetration of substances towards a lower concentration for uniform distribution of O 2 and CO 2, ions with a molecular weight of less than 500. Molecules with a higher molecular weight (proteins) do not diffuse through the membrane. They are carried by other mechanisms;
- filtration - the penetration of substances through a biomembrane under the influence of pressure equal to the difference between hydrostatic pressure (P hydr., pushing substances out of the vessels) and oncotic pressure (P onc, holding fluid in the vascular bed). In capillaries P hydr. slightly higher Ronc. If P hydr. , above P onc, filtration occurs (exit from the capillaries into the intercellular space), if it is below P onc, absorption occurs. But filtration also ensures the passage through the biomembrane of capillaries only of substances with a molecular weight of less than 5000;
- microvesicular transport or transport through large pores - the transfer of substances with a molecular weight of more than 5000 (proteins). It is carried out using the fundamental biological process of micropinocytosis. The essence of the process: microparticles (proteins) and solutions are absorbed by the biomembrane bubbles of the capillary wall and transferred through it into the intercellular space. In fact, it resembles phagocytosis. The physiological significance of micropinocytosis is evident from the fact that, according to the calculated data, in 35 minutes the endothelium of the microcirculation bed with the help of micropinocytosis can transfer a plasma volume equal to the volume of the capillary bed into the precapillary space!

10.2. Hemorheology and microcirculation

Hemorheology is the science of the influence of blood elements and their interaction with capillary walls on blood flow.

10.2.1. Influence of blood elements: interaction with each other (aggregation) and influence on blood flow

The viscosity of blood is due to the molecular forces of adhesion between the layers of blood, blood cells and the wall of blood vessels.

The greatest influence on blood viscosity is exerted by:

blood proteins and especially fibrinogen (an increase in fibrinogen increases blood viscosity);
erythrocyte hematocrit (Ht) = volume of erythrocytes in %

An increase in Ht is observed with an increase in blood viscosity. In many pathological conditions (coronary insufficiency, thrombosis), blood viscosity increases. With anemia, naturally, blood viscosity drops, as the number of red blood cells decreases.

mechanism of influence. Why do erythrocytes, as well as platelets, affect blood viscosity? On the surface of erythrocytes and platelets, there is a negative zeta potential, therefore, similarly charged erythrocytes and platelets, carrying a negative potential on their outer membrane, repel each other (the so-called electrokinetic activity). This phenomenon underlies ESR.

An increase in the content of high-molecular proteins in the blood, including fibrinogen, leads to a drop in the potential on the surface of erythrocytes, so they, repelling already weaker, aggregate into "coin columns" (ADP, thrombin, norepinephrine also act). Heparin, on the contrary, increases electrokinetic activity and accelerates blood flow in the microcirculation.

10.2.2. Influence of interaction with the capillary wall

When blood moves through the capillary, an immovable parietal layer is formed between the central moving part of the erythrocytes and the capillary wall, apparently playing the role of a lubricant.

Normally, blood cells move freely without sticking to the walls of the vessel. If the endothelium is damaged, “platelets” immediately stick to it (atherosclerosis, mechanical trauma, inflammatory damage to the walls of the capillaries).

Probably, this can be considered as a protective, homeostatic phenomenon, since platelets close the defect. With the formation of a thrombus, a dangerous restriction of blood flow, separation of a thrombus and embolism is possible, which is a pathological condition.

10.2.3. Factors regulating microcirculation

Microcirculation regulation factors are aimed at: a) changing vascular tone and b) changing permeability.

Arterioles and venules:

The nervous system and its mediators norepinephrine and acetylcholine regulate at the level of arterioles and venules. Norepinephrine has a predominantly vasoconstrictor effect, acetylcholine has a vasodilatory effect.
Endocrine system - angiotensin, vasopressin has a vasoconstrictor effect.

Precapillary sphincters:

There is no nervous regulation.
The tone and diameter are changed by local tissue hormones of mast cells and basophils during their degranulation: histamine (vasodilation and increased capillary permeability), serotonin (mainly vasoconstriction), leukotrienes (vasoconstriction), prostaglandins (prostacyclin - constriction, thromboxane A2 - dilation), kinins (vasodilation and increased permeability). All these hormones are called local, as they are formed locally, in the tissues. Their action is short-term, because they are quickly destroyed with a half-life of sec / min.

Examples of a typical development of events:

expansion of resistive vessels of microcirculation (vasodilatation) decrease in blood pressure decrease in the speed of linear blood flow - slowing down of blood flow pendulum-like movements and stopping of blood flow;
increased vascular permeability - plasma loss, blood clotting, increased viscosity, slowing blood flow, stasis. With an increase in permeability - the release of erythrocytes - hemorrhages.

10.2.3. General pathology of microcirculation

The numbering is given in accordance with the original source.

Due to the fact that microcirculation disorders are included as an important pathogenetic link in a number of typical pathological processes and in many pathological processes in organs and systems, knowledge of microcirculation disorders is necessary for physicians of various specialties.

Causes of microcirculation disorders:

intravascular changes.
Changes in the vessels themselves.
extravascular changes.

10.2.3.1. Intravascular changes as a cause of microcirculation disorders

Degranulation of basophils leads to the release of biologically active substances and heparin, which affect the tone and permeability of blood vessels and blood coagulation (in inflammatory and allergic reactions).
Disorders of the rheological properties of blood: the 1st pathogenetic mechanism is associated with intravascular aggregation of erythrocytes (sludge) and slowing of capillary blood flow. The aggregation of erythrocytes is described in the works of the 18th century on inflammation and at the beginning of the 20th century was given by the Swedish scientist Fahreus when studying the blood of pregnant women. This phenomenon underlies the definition of ESR.
In 1941-1945. Kneisli, Rloch described the extreme degree of erythrocyte aggregation - sludge (in translation - thick mud, mud, silt). It is necessary to distinguish between erythrocyte aggregation (reversible) and agglutination (irreversible) - adhesion as a result of immune conflicts.
The main signs of slugged blood are: erythrocytes, leukocytes, platelets sticking to each other and to the vessel wall, the formation of "coin columns" and an increase in blood viscosity.
Consequences of sludge: difficulty in perfusion through the microcirculation channel up to the cessation of blood flow (pendulum-like movement of blood leading to hypoxia of cells, organs). For example, with periodontal disease in the upper part of the gum at the crown.
compensatory response. In conditions of difficulty in perfusion and thrombus formation, shunting arteriolo-venular anastomoses are opened. However, full compensation does not occur and a violation of many organs develops due to hypoxia.
Pathogenetic principles of restoring the rheological properties of blood
1. The introduction of low molecular weight dextrans (polyglucin, rheomacrodex).
  Mechanism of action:
  - blood dilution (hemodilution) and an increase in oncotic pressure due to the macromolecules of these hydrocarbons, resulting in the transfer of fluid from the intercellular substance to the vessels;
  - increased zeta potential on erythrocytes, platelets;
  - closure of the damaged wall of the vascular endothelium.
2. The introduction of anticoagulants (heparin), which increase the zeta potential on the membranes of erythrocytes, platelets, leukocytes.
3. The introduction of thrombolytics (fibrinolysin).

We considered one of the intravascular causes of microcirculation disorders - erythrocyte aggregation, and the second cause associated with disseminated intravascular coagulation (DIC) when tissue coagulation reaction factors enter the bloodstream with the development of intravascular coagulation, we will analyze in Chapter 19.

Most pathological conditions are accompanied by intravascular coagulation. When tissues are destroyed, tissue thromboplastin is washed out of them into the vascular bed (the placenta and parenchymal organs are especially rich in it). Once in the bloodstream, it triggers a blood coagulation reaction, which is accompanied by the formation of fibrin clots, blood clots. This reaction limits blood loss, therefore, it refers to reactions of a protective, homeostatic nature.

10.2.3.2. Microcirculation disorders associated with pathological changes in the vascular wall

Types of pathological changes in the walls of blood vessels:

increased permeability of capillary membranes associated with the action of biologically active substances (histamine, kinins, leukotrienes) during fever, inflammatory, immune and other damage. Due to the action of diffusion and filtration forces, this leads to a significant increase in the loss of plasma, and with it substances with a molecular weight of more than 5000, an increase in blood viscosity and progressive aggregation of red blood cells. Stasis occurs, leading to tissue edema;
the extreme degree of high permeability is damage to the biomembranes of the walls of microvessels and adherence of blood cells to them. After 5-15 minutes, platelet adhesion is detected in the area of damage. Adhering platelets form a "pseudoendothelium" that temporarily covers a defect in the endothelial wall (platelet lining). With more severe damage to the vascular wall, diapedesis of blood cells and microhemorrhage occur.

10.2.3.3. Microcirculation disorders associated with perivascular changes

The microcirculation system with its central part - capillaries - is a single functional whole with the cells of the parenchyma and stroma of the organ.

The role of tissue mast cells in microcirculation disorders under the influence of pathological factors

Mast cells, due to the fact that they are located next to microvessels or directly in them (basophils), have the greatest influence on the microcirculation system. This is due to the fact that they are a depot of biologically active substances (local tissue hormones). Their usual reaction to a damaging factor is degranulation, accompanied by the release of biologically active substances and heparin. The effect of biologically active substances on microcirculation is associated with an effect on the tone and permeability of microvessels, and heparin - with an anticoagulant effect;

Difficulty in lymphatic circulation

Lymphatic capillaries play a drainage role. When lymphatic capillaries are deformed, for example, when acute inflammation passes into chronic inflammation, obliteration (infection) of the lymphatic capillaries occurs. Violation of the outflow of fluid and protein, an increase in tissue pressure in the intercellular fluid leads to difficulty in microcirculation, the transition of the liquid part of the blood from the bloodstream to the tissues, which is essential in the development of edema in the lesion.

10.2.4. Violation of microcirculation in typical pathological processes

Typical pathological processes include pathological reactions that occur in the same way in animals and humans. On the one hand, this proves our common evolutionary origin, on the other hand, it allows scientists to transfer the results of experiments from animals to humans. Typical pathological processes include, for example:

inflammation:
immune disorders:
tumor growth;
ionizing radiation.

10.2.4.1. Microcirculation disorders in local tissue damage

The result of the local effect of any pathological agent on the tissue is damage to the membranes of lpsosomes, the release of their enzymes, causing excessive formation of biologically active substances, for example, kinins, or through the degranulation of mast cells, basophils. Since these are microcirculation regulators, any process that causes an increase in biologically active substances will cause microcirculation disorders.

10.2.4.2. Inflammation and microcirculation disorders

Like no other process, inflammation is associated with microcirculation disorders. BAS cause:

arterial vasodilation in the focus of inflammation (hyperemia);
increased permeability in the focus (edema, increased blood viscosity, mainly in venules, diapedesis of erythrocytes - microhemorrhages, leukocytes);
adhesion of platelets to the walls of the endothelium (thrombus);
erythrocyte aggregation (blood flow slowdown, stasis, sludge formation, hypoxia);

In the final stage of inflammation - proliferation - the need for amino acids, oxygen for ATP biosynthesis is increased, which is prevented by microcirculation disorders. Therefore, it is very important to restore effective blood flow in the healing early.

10.2.4.3. Burn injury and microcirculation

Since the action of the thermal factor also leads to damage to the lysosome membranes (the trigger for inflammation), this problem turns into a more general problem of inflammation, in this case, non-infectious inflammation.

At first, in the focus of the burn, venules are mainly damaged, as in inflammation. After a few hours, permeability changes develop predominantly in the capillaries. Erythrocyte aggregation develops ("coin columns" or "granular caviar"), leading to stasis, sludge and hypoxia. This state of impaired microcirculation, in essence, underlies the burn shock.

10.2.4.4. HCNT and HCRT and microcirculation

The described general pathological regularity in the development of microcirculation disorders can also be traced in allergic reactions. The site of antigen-antibody or antigen-killer T-lymphocyte reactions can be the microcirculation system. And again, the degranulation of tissue mast cells and blood basophils under the influence of the immune complex with the release of biologically active substances and heparin plays an important role here. The release of these substances leads to pathochemical disorders, as a result of which a complex of severe pathophysiological disorders develops - a state of shock.

We analyzed 3 typical pathological processes: inflammation, burns, allergic reactions. All of them in the initial phases have their own specifics: etiology and pathogenesis. But now no one doubts that microcirculation disorders and, ultimately, organ perfusion play a significant role in the pathogenesis and outcome of inflammatory and shock syndromes.

Stasis: types, causes, manifestations, consequences.

Staz - a significant slowdown or cessation of blood and / or lymph flow from the vessels of an organ or tissue.

Causes

Ischemia and venous hyperemia. They lead to stasis due to a significant slowdown in blood flow (during ischemia due to a decrease in arterial blood flow, with venous hyperemia as a result of slowing or stopping its outflow) and creating conditions for the formation and / or activation of substances that cause the gluing of blood cells, the formation of them aggregates and thrombi.

Proaggregants are factors that cause aggregation and agglutination of blood cells.

Stasis pathogenesis:

At the final stage of stasis, there is always a process of aggregation and / or agglutination of blood cells, which leads to thickening of the blood and a decrease in its fluidity. This process is activated by proaggregants, cations and high molecular weight proteins.

Proaggregants (thromboxane A 2, catecholamines AT to blood cells) cause adhesion, aggregation, agglutination of blood cells with their subsequent lysis and release of BAB from them.

Cations. K + , Ca 2+ , Na + , Mg 2+ are released from blood cells, damaged walls of blood vessels and tissues. Being adsorbed on the cytolemma of blood cells, the excess of cations neutralizes their negative surface charge.

High-molecular proteins (for example, γ-globulins, fibrinogen) remove the surface charge of intact cells (by connecting to the negatively charged cell surface with the help of positively charged amino groups) and potentiate the aggregation of blood cells and the adhesion of their conglomerates to the vessel wall.

Types of stasis

Primary (true) stasis. The formation of stasis primarily begins with the activation of blood cells and the release of a large number of proaggregants and/or procoagulants. At the next stage, formed elements aggregate, agglutinate and attach to the wall of the microvessel. This causes a slowdown or cessation of blood flow in the vessels.

Secondary stasis (ischemic and congestive).

Ischemic stasis develops as an outcome of severe ischemia due to a decrease in arterial blood flow, a slowdown in the rate of its current, and its turbulent nature. This leads to aggregation and adhesion of blood cells.

Congestive (venous-congestive) variant of stasis is the result of a slowdown in the outflow of venous blood, its thickening, changes in physicochemical properties, damage to blood cells (in particular, due to hypoxia). Subsequently, blood cells adhere to each other and to the wall of microvessels.

Manifestations of stasis

At stasis characteristic changes occur in the vessels of the microvasculature:

a decrease in the inner diameter of microvessels in ischemic stasis, an increase in the lumen of the vessels of the microcirculatory bed in congestive stasis, a large number of aggregates of blood cells in the lumen of blood vessels and on their walls, microhemorrhages (more often with congestive stasis).

Consequences of stasis:

With the rapid elimination of the cause of stasis, blood flow in the vessels of the microvasculature is restored and no significant changes develop in the tissues.

Prolonged stasis leads to the development of dystrophic changes in tissues, often to the death of a tissue or organ site (heart attack).

Sludge: characteristics of the concept, causes, mechanisms of formation, manifestations and consequences.

Sludge- a phenomenon characterized by adhesion, aggregation and agglutination of blood cells, which causes its separation into conglomerates of erythrocytes, leukocytes, platelets and plasma, as well as impaired microcirculation.

Causes of Sludge:

Violation of central hemodynamics (with heart failure, venous congestion, pathological forms of arterial hyperemia).

Increased blood viscosity (for example, in conditions of hemoconcentration, hyperproteinemia, polycythemia).

Damage to the walls of microslums (with local pathological processes, allergic reactions, tumors)

Sludge Development Mechanisms:

FEK - formed elements of blood.

Sludge effects:

1. Violation of blood flow inside the vessels (slowdown, up to stasis, turbulent blood flow, inclusion of arteriovenular shunts), disorder of the processes of transcapillary flow of blood cells.

2. Violation of metabolism in tissues and organs with the development of dystrophies and the breakdown of plastic processes in them.

Causes: metabolic disorders of 0 2 and CO 2 due to adhesion and aggregation of erythrocytes and the development of vasculopathy as a result of the cessation or significant decrease in the angiotrophic function of platelets (they are in conglomerates of blood cells).

3. Development of hypoxia and acidosis in tissues and organs.

Sludge Phenomenon is the cause of microcirculation disorders (in cases where it develops primarily) or a consequence of intravascular microcirculation disorders (in their primary development).

Microcirculation disorders: causes, typical forms. Intravascular disorders: main forms, causes, manifestations and consequences.

microcirculation- ordered movement of blood and lymph through microvessels, transcapillary transfer of plasma and blood cells, movement of fluid in the extravascular space.

Microcirculatory bed. The totality of arterioles, capillaries and venules constitutes the structural and functional unit of the cardiovascular system - the microcirculatory (terminal) bed. The terminal bed is organized as follows: from the terminal arteriole, the metarteriole departs, breaking up into anastomosing true capillaries forming a network; the venous part of the capillaries opens into postcapillary venules. At the site of separation of the capillary from the arterioles, there is a precapillary sphincter - an accumulation of circularly oriented SMCs. Sphincters control the local volume of blood passing through the true capillaries; the volume of blood passing through the terminal vascular bed as a whole is determined by the tone of the SMC arterioles. In the microvasculature, there are arteriole-venular anastomoses that connect arterioles directly with venules or small arteries with small veins (juxtacapillary blood flow). The wall of the anastomotic vessels contains many SMCs. Arteriovenous anastomoses are present in large numbers in some areas of the skin, where they play an important role in thermoregulation (earlobe, fingers). The microvasculature also includes small lymphatic vessels and intercellular space.

Causes of microcirculation disorders.

Numerous causes that cause a variety of microcirculation disorders are grouped into three groups.

Disorders of the central and regional circulation. The most significant include heart failure, pathological forms of arterial hyperemia, venous hyperemia, ischemia.

Changes in the viscosity and volume of blood and lymph. Develop due to hemo-concentration and hemodilution.

Hemo (lymph) concentration. Causes: hypohydration of the body with the development of polycythemic hypovolemia, polycythemia, hyperproteinemia (mainly hyperfibrinogenemia).

Hemo(lymph) dilution. Causes: hyperhydration of the body with the development of oligocythemic hypervolemia, pancytopenia (decrease in the number of all blood cells), increased aggregation and agglutination of blood cells (leads to a significant increase in blood viscosity), DIC.

Damage to the walls of the vessels of the microvasculature. Usually observed in atherosclerosis, inflammation, cirrhosis, tumors, etc.

Standard forms intravascular (intravascular) disorders:

1. Slowdown (up to stasis) of blood and/or lymph flow.

The most common causes:

A) Disorders of hemo- and lymphodynamics (for example, with heart failure, venous hyperemia, ischemia).

B) An increase in blood and lymph viscosity [as a result of hemo (lymph) concentration with prolonged vomiting, diarrhea, plasmorrhagia with burns, polycythemia, hyperproteinemia, aggregation of blood cells, its intravascular coagulation, microthrombosis).

C) A significant narrowing of the lumen of microvessels (due to their compression by a tumor, edematous tissue, the formation of blood clots in them, embolism, swelling or hyperplasia of endothelial cells, the formation of an atherosclerotic plaque, etc.).

Manifestations. Similar to those observed in the vessels of the microvasculature in venous hyperemia, ischemia or stasis.

2. Acceleration of blood flow.

Main reasons.

A) Hemodynamic disorders (for example, with arterial hypertension, pathological arterial hyperemia, or discharge of arterial blood into the venous bed through arteriovenular shunts).

B) Decreased blood viscosity due to hemodilution (with water poisoning); hypoproteinemia, renal failure (with oliguric or anuric stage); pancytopenia.

3. Violation of laminarity (turbulence) of blood and/or lymph flow.

The most common reasons.

A) Changes in the viscosity and aggregate state of the blood (as a result of the formation of aggregates of blood cells in polycythemia, a significant increase in the number of blood cells above the norm or hyperfibrinogenemia; with the formation of microthrombi).

B) Damage to the walls of microvessels or a violation of their smoothness (with vasculitis, cell hyperplasia

endothelium, arteriosclerosis, fibrotic changes in various layers of the vascular walls, the development of tumors in them, etc.)

4. Increased juxtacapillary blood flow. Occurs due to the opening of arteriovenular shunts and the discharge of blood from arterioles into venules, bypassing the capillary network of the microvasculature. Cause: spasm of SMC arterioles and closure of precapillary sphincters with a significant increase in the level of catecholamines in the blood (for example, during a hypercatecholamine crisis in patients with pheochromocytoma), an excessive increase in the tone of the sympathetic nervous system (for example, under stress), a hypertensive crisis (for example, in patients with essential hypertension ). Manifestations: ischemia in the region of blood discharge from arterioles to venules, opening and / or increase in the diameter of arterio-venular shunts, Turbulent nature of the blood flow in the places of branches and entrances to the venules of the shunting vessels (due to the fact that arterio-venular shunts depart from arterioles and flow into venules, as a rule, at a significant angle; this is accompanied by a collision of blood cells with each other and the vessel wall, which leads to the release of proaggregants and procoagulants, to the formation of aggregates and blood clots)

MICROCIRCULATION DISORDERS

It is generally recognized that there are three interconnected links in the cardiovascular system: arterial, venous and the capillary linking them - established in our ideas with the light hand of M. Malpighi, who supplemented the great discovery by W. Harvey (1628) of the circulatory system, with an equally significant description of the "missing "Harvey in the circulatory system link - capillaries (1661).

However, until the beginning of the 20th century, the focus was on the study of the heart and large blood vessels. And the “connecting” itself, “the missing link between arteries and veins is the capillary system, which includes almost 90% of all blood vessels,

For many years it did not attract due attention. At the same time, it is the capillary bed that ensures the processes of metabolism and the vital activity of organs and tissues, which determines their truly central role in the system for ensuring tissue homeostasis, as well as in the development of many pathological processes.

So, under microcirculation understand the ordered movement of blood and lymph through microvessels, the transcapillary exchange of oxygen, carbon dioxide, metabolic substrates and its products, ions, biologically active substances, as well as the movement of fluid in the extravascular space.

In a broad sense, the concept of "microcirculation" also includes the movement of fluid through the cell membrane and its circulation in the cell. There is information about the orderly movement of a liquid of different composition in various parts of the hyaloplasm, as well as cell organelles.

The vessels of the microvasculature include arterioles, precapillaries, capillaries, postcapillary venules (postcapillaries), venules, arteriovenular shunts, and lymphatic vessels.

The diameter of the vessels of the microvasculature varies from 2 to 200 microns.

Arterioles are the main components of resistive vessels. The tone of their muscle wall is regulated by the sympathetic and parasympathetic nervous system, as well as BAS. Arterioles provide regulation of the volume of blood supply to tissues and laminar blood flow.

Precapillaries are also involved in the regulation of tissue blood supply by changing the lumen of precapillary sphincters formed by smooth muscle cells. The tone of their walls is regulated by nervous influences and humoral factors.

The trophic, exchange component of the microvasculature is made up of capillaries with a diameter of 2 to 20 microns. The processes of exchange of oxygen, carbon dioxide, substrates and products of metabolism, ions, biologically active substances directly proceed in them. All these complex and diverse processes are mainly regulated by agents of local (regional) origin: prostaglandins, kinins, biogenic amines, adenine nucleases, ions, etc. These and other factors also regulate the lumen of capillaries by changing the volume of endothelial cells and the tone of pericytes.

Postcapillaries and venules are blood collectors. Their capacity significantly exceeds the total capacity of arterioles and precapillaries. They regulate the volume of outflowing blood and indirectly - its inflow to the tissues, tissue turgor.

Arteriovenular anastomoses are involved in the regulation of blood flow volume and tissue blood supply. Opening them contributes to the mobilization of deposited blood.

Through the lymphatic capillaries and vessels, lymph is transported to the lymphatic trunks and then to the venous system.

Common causes of microcirculation disorders.

As you know, microcirculation disorders are included as an important pathogenetic link in a number of typical pathological processes and in many particular forms of various diseases, therefore, when analyzing the relevant sections, we will also cover issues related to these disorders.

Microcirculation disorders are usually divided into intravascular disorders associated with the violation of the vessels themselves, transmural extravascular changes.

Numerous causes that directly cause a variety of disorders can be grouped into three groups:

1. Disorders of the central and peripheral circulation. Among the most important among them are heart failure, pathological forms of arterial hyperemia, venous hyperemia and ischemia.

2. Changes in the viscosity and volume of blood and lymph. They can develop as a result of the following reasons:

a) hemo (lymph) concentrations, which may be the result of hypohydration, polycythemia, hyperproteinemia (hyperfibrinogenemia)

b) hemo (lymph) dilution, which can develop as a result of hyperhydration, pancytopenia, hypoproteinemia.

c) aggregation and agglutination of blood cells, accompanied by an increase in blood viscosity,

d) intravascular disseminated blood coagulation, fibriolysis and thrombosis.

3. Damage to the walls of the vessels of the microvasculature, causing a violation of their integrity and smoothness. This is usually observed in atherosclerosis, inflammation, cirrhosis, tumors, etc.

Intravascular disorders

Among intravascular pathological disorders of microcirculation, one of the first places should be aggregation of erythrocytes and other blood cells. Other intravascular disorders, such as impaired blood flow velocity or thromboembolism, also often depend on a fall in the normal stability of blood suspensions.

The preservation of the suspension stability of blood is ensured by the magnitude of the negative charge of erythrocytes and platelets, a certain ratio of protein fractions (albumin, on the one hand, and globulins and fibrinogen, on the other). A decrease in the negative surface charge of erythrocytes, as well as an absolute or relative increase in the content of positively charged macromolecules of globulins and fibrinogen and their adsorption on the surface of erythrocytes. May lead to a decrease in the suspension stability of blood, to the aggregation of erythrocytes and other blood cells. A decrease in blood flow speed exacerbates this process.

In 1918, the Swedish scientist Fahraeus, in his work on the study of the blood of women during pregnancy, showed that in this condition, the formation of erythrocyte aggregates and the acceleration of the sedimentation of the latter take place. On the basis of these and his other works, he proposed to use the erythrocyte sedimentation reaction (ERS) or the determination of the erythrocyte sedimentation rate (ESR), which is now widespread in the practice of medicine. Acceleration of ESR is usually associated with an increase in the plasma concentration of coarse proteins.

The phenomenon of erythrocyte aggregation is reflected in such a phenomenon as sludge (the term "sludge" itself literally translated from English means mud, or thick mud, silt).

The sludge phenomenon is characterized by adhesion, aggregation and agglutination of blood cells, which causes its separation into more or less large conglomerates consisting of erythrocytes, platelets, leukocytes and plasma.

The causes of sludge are the same factors that cause microcirculation disorders:

1) violation of the central and regional hemodynamics in heart failure, venous congestion, ischemia, pathological arterial hyperemia.

2) an increase in blood viscosity in conditions of blood clotting, hyperproteinemia, polycythemia.

3) damage to the walls of microvessels.

The action of these factors determines the aggregation of blood cells, mainly erythrocytes, their adhesion to each other and microvascular endothelial cells, cell agglutination followed by lysis of their membranes - cytolysis.

To the number main mechanisms adhesion, aggregation and agglutination of blood cells, leading to the development of sludge, include

1) activation of blood cells under the influence of these causative factors, followed by the release of physiologically active substances from them, including those with a proaggregative effect. These include ADP, thromboxane A 2, kinins, histamine, a number of prostaglandins. 2) "removing" the negative surface charge of the cells or "recharging it to a positive one.

The presence and magnitude of the negative surface charge of blood cells are important conditions for ensuring its suspension stability. The latter is determined by the action of repulsive forces between similarly charged blood cells. An increase in plasma cations of potassium, calcium, magnesium, etc. reduces the surface charge of blood cells or changes it to "+". Cells approach each other, the process of their adhesion, aggregation and agglutation begins, followed by blood separation. The latter disrupts the exchange of oxygen, carbon gas, substrates and metabolic products between blood and tissues.

3) a decrease in the magnitude of the surface charge of the cellular elements of the blood upon contact with them of protein macromolecules during hyperproteemia, especially due to its high molecular weight fractions (immunoglobulins, fibrinogen, abnormal proteins). In this case, the surface charge decreases due to the interaction of cells with positively charged protein macromolecules, in particular, with its amino groups. In addition, protein micelles, being adsorbed on the surface of cells, promote their connection and subsequent adhesion, aggregation and agglutination. The formation of aggregates of blood cells is accompanied by its separation into cell conglomerates and plasma.

Depending on the nature of the impact, sludge can be reversible (if only erythrocyte aggregation is present) or irreversible. In the latter case, agglutination of blood cells occurs.

Depending on the size of the aggregates, the nature of their contours and the packing density of blood cells, the following types of sludge are distinguished:

classical (comparatively large aggregates with dense packing of erythrocytes and uneven contours). This type of sludge develops when an obstruction (such as a ligature) interferes with the free movement of blood through a vessel.

At dextrin type sludge (occurs when dextran with a large molecular weight of 250,000-500,000 and more is introduced into the blood) aggregates have a different size, dense packing, rounded outlines, free spaces in the form of cavities.

Allocate also amorphous type sludge, which is characterized by the presence of a huge number of small aggregates, similar to granules. In this case, the blood takes the form of a coarse liquid. The amorphous type of sludge develops when ethyl alcohol, ADP and ATP, thrombin, serotonin, norepinephrine, etc. are injected into the blood.

The sizes of the aggregates vary widely depending on the diameter of the vessels. The small size of aggregates in amorphous sludge can be no less, but even the greatest danger to microcirculation, since their size allows them to penetrate into the smallest vessels up to and including capillaries. Larger aggregates, depending on the degree of their compaction, can move through the vessels, or cause embolism of vessels of a smaller diameter.

Consequences.

The sludge phenomenon is accompanied by a narrowing of the lumen and impaired perfusion of microvessels (slowing of blood flow in them, up to stasis, turbulent nature of blood flow), a disorder in the processes of transcapillary metabolism, the development of hypoxia and acidosis, and metabolic disorders in tissues. In general, the combination of these changes is referred to as the syndrome of capillary-trophic insufficiency.

Thus, the sludge phenomenon, which initially appears as a local reaction of the tissue to damage, in its further development can acquire the character of a systemic reaction, a generalized response of the body. This is its general pathological significance.

Intravascular coagulation disorders are mainly associated with the reaction of platelets and fibrinogen to tissue damage. Platelets, both local and in the general circulation, react quite quickly to tissue damage. It has been established that platelet aggregation and acceleration of blood coagulation can be caused by: tissue necrotization (tissue thromboplastin), adenosine diphosphate is released when tissues are damaged, bacteria, viruses, antigen-antibody complex, endotoxins, trypsin-type enzymes, and other factors.

Serious changes in microcirculation may be associated with a violation of the ratio between blood coagulation and fibrinolysis that occurs when tissues are damaged.

Change in blood flow velocity(its increase or decrease) within functional limits is a common physiological phenomenon. Slowdown until the cessation of blood and lymph flow may be due to the following factors:

1) disorders of hemo and lymphodynamics in heart failure, venous hyperemia, ischemia.

2) an increase in the viscosity of blood and lymph as a result of thickening of the blood with prolonged vomiting, diarrhea, plasmorrhagia with burns, polycythemia, hyperproteemia, thrombosis.

3) a significant narrowing of the lumen of microvessels due to their compression by a tumor, edematous tissue, the formation of a thrombus, embolus in them, swelling or hyperplasia of endothelial cells, the formation of an atherosclerotic plaque, etc.

Slowing blood flow causes underperfusion of the microvasculature, which is essential pathogenetic link all processes accompanied by a drop in perfusion pressure in the microvascular bed. The consequence of this may be hypoxia, and with complete stasis - tissue anoxia with all the ensuing consequences.

Acceleration of blood flow and lymph can cause the following reasons: violations of hemo- and lymphodynamics, for example, when arterial blood is discharged into the venous bed through arteriovenular shunts;

Decrease in blood viscosity (with water poisoning due to hemodilution, pancytopenia, hypoproteinemia, renal failure.

PATHOLOGICAL REACTIONS AT THE LEVEL OF THE VASCULAR WALL

Given that blood plasma and lymph are transported through the vascular wall, as well as blood cells, transmural (“transwall”) microcirculation disorders are divided into two main subgroups: changes in fluid flow and movement of blood cells. The volume of fluid transported through the wall of the vessel under various pathological conditions can either increase or decrease significantly compared to the proper one.

Increasing the volume of transported liquid. The basis of this phenomenon is an excessive increase in the permeability of the vascular wall. Among the most significant reasons are: a decrease in oxygen pressure, an increase in carbon dioxide pressure, a local decrease in pH associated with the accumulation of metabolites, such as lactic acid (this contributes to the non-enzymatic hydrolysis of the components of the basement membrane of blood vessels, "loosening" it and, as a result, easier plasma flow under conditions of acidosis, lysosome hydrolases and enzymes are activated, which causes enzymatic hydrolysis of the components of the basement membrane of blood vessels). In addition, the action of biogenic amines - histamine, serotonin, bradykinin, causing contraction of endothelial cells and expansion of the gaps between them. Among the reasons for the increase in capillary permeability, one can also name such as violation of the integrity of the vessel wall - the formation of microfractures, stretching of the fenestra. This is often observed in conditions of overflow of the vessels of the microvasculature with blood during venous stasis or lymph (with lymphostasis). An increase in the permeability of the vascular membrane under the influence of these factors significantly potentiates the mechanisms of fluid transport:

a/ filtration - fluid transport along a hydrostatic pressure gradient;

b/ microvesiculation (invagination of the endothelial wall with the capture of a "quantum" of plasma, the formation of a vesicle, its migration to the basal side of the cell, the "opening" of the vesicle and the "ejection" of fluid on the opposite side of the cell surface);

c/ diffusion.

Reducing the volume of transported fluid. This phenomenon is based on a significant decrease in the permeability of the vascular wall. The reason is the thickening or thickening of the vascular wall, which develop due to the accumulation of excess calcium salts / calcification / and excessive formation of fibrous structures and glycosaminoglycans in the wall, cell hypertrophy and hyperplasia, tissue and vascular wall edema.

Thickening, compaction of the vascular wall and, as a result, a decrease in vascular permeability prevents the implementation of the mechanisms of fluid transport - filtration, diffusion and microvesiculation - and thereby causes a decrease in the volume of its transmural transfer.

Change in the volume of transport of blood cells. Considering that the transport of a certain number of leukocytes and, to a lesser extent, platelets through the vascular wall is carried out normally, the pathology of the transport of blood cells mainly refers to their excessive exit outside the vessel, especially erythrocytes: pathological diapedesis.

main reason This phenomenon is a significant increase in permeability or a violation of the integrity of the vascular wall. A significant increase in diapedesis of leukocytes, erythrocytes and platelets is observed with inflammation, allergic reactions, intoxication with endo- and exotoxins of bacteria, and exposure to penetrating radiation.

Diapedesis of erythrocytes also increases in conditions of thrombocytopenia. Platelets have been shown to have an angiotrophic effect. A decrease in their number of blood causes dystrophy and death of endothelial cells, an increase in the permeability of the walls of microvessels. On the contrary, with thickening or compaction of the walls of microvessels in any region of the tissue, the “scale” of the release of leukocytes into this tissue, where they participate in the implementation of immune surveillance reactions, may decrease. As a result, the effectiveness of local immunity is reduced.

Extravascular disorders, as a rule, consist in a more or less pronounced slowing of the flow of the intercellular fluid and, often in connection with this, an increase in the volume of water in the extravascular space due to an obstacle to the outflow of fluid into the lymphatic vessels and venules. Less commonly, there is a decrease in the volume of the intercellular fluid, for example, with dehydration or a decrease in lymph formation, which can also be combined with a decrease in the rate of its flow.

Main reasons Extravascular microcirculation disorders are local pathological processes that develop in connection with inflammation, allergic reactions, tumor growth, impaired neurotrophic influences, and disorders of lymph formation.

Among the main direct factors causing difficulty in the flow of intercellular fluid include the narrowing of intercellular gaps (in particular, due to overhydration and swelling of cells).

An increase in viscosity of a liquid (for example, with an increase in the content of proteins, lipids, metabolites in it.

Embolism of the lymphatic capillaries.

Decreased efficiency of water reabsorption in postcapillaries and venules. A decrease in the volume of interstitial fluid and a slowdown in its flow may be the result of a decrease in filtration pressure in arterioles or an increase in fluid reabsorption in venules.

P atogenetic value.

Regardless of the reasons for the obstruction of the intercellular fluid flow in the tissues, the content of products of normal and impaired metabolism, ions, biologically active substances increases, cell compression is observed, transmembrane transport of oxygen, carbon gas, metabolic products, ions is disturbed, which in turn can cause cell damage. In general, with any microcirculation disorders, especially with their prolonged course, a syndrome of capillary-trophic insufficiency develops. It is characterized by: 1) a violation of the transport of intercellular fluid, as well as perfusion of lymph and blood through microvessels, 2) a disorder in the exchange of oxygen, carbon gas, substrates and metabolic products, ions, PAS in the capillaries. 3) metabolic disorders in cells. This, in turn, causes the development of various variants of dystrophic changes in tissues and organs, disruption of plastic processes in them and disorders of their vital activity.

All systems, organs and tissues of the body function by obtaining the energy of ATP, which, in turn, can be formed in sufficient quantities in the presence of oxygen. How does oxygen get into organs and tissues? It is transported with the help of hemoglobin through the blood vessels, which form a microcirculation or microhemodynamics system in the organs.

Levels of the circulatory system

Conventionally, all blood supply to organs and systems of the body can be divided into three levels:

Microcirculation: what is it?

Microcirculation is the movement of blood along the microscopic, that is, the smallest, part of the vascular bed. There are five types of vessels that are part of it:

arterioles;
precapillaries;
capillaries;
postcapillaries;
venules.

Interestingly, not all vessels of this channel function simultaneously. While some of them are actively working (open capillaries), others are in "sleep mode" (closed capillaries).

The regulation of the movement of blood through the smallest blood vessels is carried out by contraction of the muscular wall of the arteries and arterioles, as well as the work of special sphincters, which are located in the postcapillaries.

Structural features

The microcirculatory bed has a different structure, depending on which organ it is located in.

For example, in the kidneys, the capillaries are collected into a glomerulus, which is formed from the afferent artery, and the efferent artery is then formed from the glomerulus of capillaries itself. Moreover, the diameter of the afferent is twice as large as that of the efferent. This structure is necessary for blood filtration and the formation of primary urine.

And in the liver are wide capillaries called sinusoids. Both oxygenated arterial and poor venous blood enter these vessels from the portal vein. Special sinusoids are also present in the bone marrow.

Functions of microcirculation

Microcirculation is a very important part of the vascular bed, performing the following functions:

exchange - the exchange of oxygen and carbon dioxide between the blood and cells of internal organs;
heat exchange;
draining;
signal;
regulatory;
participation in the formation of color and consistency of urine.

Pathological conditions

The blood flow in the microcirculatory bed depends on the constancy of the internal environment of the body. Including the normal function of blood vessels is most affected by the work of the heart and endocrine glands. However, other internal organs also have influence. Therefore, the state of microcirculation reflects the work of the body as a whole.

Conventionally, all pathological conditions of the vessels of the microvasculature can be divided into three groups:

Intravascular changes

Slowing of blood flow in the vessels, which can manifest itself both in specific diseases, thrombocytopathies (impaired platelet function) and coagulopathy (blood clotting disorders), and in pathologies that can occur in various diseases of the body. These conditions include erythrocyte aggregation and sludge syndrome. In fact, these two processes are successive stages of one phenomenon.

First, there is a temporary attachment of red blood cells using surface contacts in the form of a column (erythrocyte aggregation). This condition is reversible and usually short-lived. However, its progression can lead to strong gluing (adhesion) of blood cells, which is already irreversible.

This pathology is called the sludge phenomenon. This leads to a slowdown and complete cessation of blood flow in the vessel. Venules and capillaries are usually clogged. The exchange of oxygen and nutrients stops, which further causes ischemia and tissue necrosis.

Destruction of the vascular wall

Violation of the integrity of the vessel wall can occur both in pathological conditions of the whole organism (acidosis, hypoxia), and in direct damage to the vessel wall by biologically active agents. In the role of such agents act in vasculitis (inflammation of the vascular wall).

If the damage progresses, seepage (diapedesis) of erythrocytes from the blood into the surrounding tissues and the formation of hemorrhages are noted.

Extravascular disorders

Pathological processes in the body can affect microcirculation vessels in two ways:

The reaction of tissue basophils, which release biologically active agents and enzymes into the environment that directly affect the vessel and thicken the blood in the vessels.
Violation of the transport of tissue fluid.

Thus, microcirculation is a complex system that is in constant interaction with the entire body. It is necessary to know not only the main types of its violations, but also the methods of diagnosis and treatment of these diseases.

Violation of microhemodynamics: diagnosis

Depending on the affected organ, various methods of instrumental diagnostics can be used, which can indirectly indicate the presence of microcirculation disorders through the pathology of the internal organ:

Violation of microhemodynamics: treatment

To improve microcirculation, a group of drugs called angioprotectors is used. These are highly effective drugs that improve blood flow through the vessels and restore the vessel itself. Their main properties are:

reduction of spasm of arteries;
ensuring the patency of the vessel;
improvement of rheology (viscosity) of blood;
strengthening of the vascular wall;
anti-edematous effect;
improvement of metabolism, that is, metabolism, in the vascular wall.

The main drugs that improve microcirculation include the following:

It can be concluded that, despite their small size and diameter, microhemodynamic vessels perform a very important function in the body. Therefore, microcirculation is a self-sufficient system of the body, the state of which can and should be given special attention.

microcirculation(from Greek mikros - smallest, lat. circulatio - arc movement) is the movement of blood and lymph through arterioles, precapillaries, capillaries, postcapillaries, venules, arteriovenous anastomoses (shunts) and lymphatic capillaries.

The circulatory system is closed. Lymphatic capillaries are blind collectors through which lymph enters the lymphatic network and is directed to the venous system through the thoracic (ductus thoracicus) and other ducts. Thus, the concept of microcirculation includes the movement of fluid between the circulatory and lymphatic capillary networks, through intracellular systems, the transmembrane exchange of gases, substrates and metabolic products, and signal molecules.

Microcirculation disorders are caused by numerous factors, which include circulatory disorders of cardiac and vascular origin (hypotension, hypertension, arterial and venous hyperemia, ischemia), violation of the integrity of the walls of the vessels of the microvasculature and the rheological properties of blood.

Typical microcirculation disorders include intravascular disorders, pathological changes in vascular permeability, and extravascular disorders.

Intravascular, or intravascular, microcirculation disorders are caused by a slowdown or cessation of blood or lymph flow. The suspension stability of blood cells, due to the negative charge of erythrocytes and platelets, is disturbed as a result of the release of albumin from the vessels. An absolute or relative increase in the content of positively charged micromolecules of fibrinogen and globulins in the blood plasma, their adsorption on the surface of blood cells leads to destabilization of the suspension, aggregation of erythrocytes, platelets, leukocytes. Vasoconstriction, an increase in viscosity, a disorder of hemo- and lymphodynamics, hindering blood perfusion through microvessels, promotes intravascular cell aggregation. The so-called "sludge phenomenon" (from English, sluge - thick mud, mud) is developing. Intravascular formation of aggregates from erythrocytes, platelets, leukocytes is observed in many infectious diseases, with frostbite and burns, shock of various origins, acute vascular insufficiency (collapse), poisoning, diseases accompanied by albuminuria, in the postoperative period.

Blood slugging develops sequentially and begins with platelet aggregation with chylomicrons (lipid particles), and subsequently with erythrocytes. Aggregation is accompanied by adhesion (adhesion) of cells among themselves and with vascular endothelial cells, agglutination (gluing) of blood cells and cytolysis.

There are the following types of sludge:

ü classic, with large cell aggregates, dense packing, uneven outlines;

ü dextran - aggregates of cells of various sizes, with dense packing and rounded outlines;

ü amorphous, representing multiple granules consisting of several erythrocytes.

Aggregation of erythrocytes leads to narrowing of the lumen of blood vessels, complete or partial obstruction (blockage) of capillaries, slowing down of blood flow, and turbulent nature of blood flow. Blockage of microvessels by erythrocyte aggregates leads to the fact that they become only plasma. Released by damaged cells histamine, serotonin, bradykinin increase the permeability of histohematic barriers; hypoxia and acidosis damage the vascular walls, creating conditions for the occurrence of multiple microthrombi. The severity of microcirculatory disorders increases. There comes a syndrome of capillary-trophic insufficiency, characterized by metabolic disorders, trophic provision of the functional activity of cells, organs, tissues, a generalized reaction of the body.

Timely elimination of the causes of sludge, blockade of the mechanisms of its formation contribute to cell disaggregation, restoration of blood flow and normalization of metabolic processes.

Permeability disorders of the vessels of the microvasculature, or transmural (from Latin trans - through, English, mural - wall), are characterized by impaired transport of substances and movement of formed elements.

Under conditions of pathology, the structure of the vascular wall changes. Its permeability for plasma and macromolecular substances can be reduced or increased. Most often, changes in the structure are accompanied by an increase in the permeability of histohematic barriers and an increase in the volume of fluid entering the intercellular spaces.

Permeability increases due to:

Ø contraction of endotheliocytes and expansion of intercellular channels;

Ø stretching of the fenestra, the occurrence of microtraumas, violations of the integrity of the walls;

Ø influence on the contact elements of the vessels of histamine, serotonin, bradykinin;

Ø enzymatic hydrolysis of the basement membrane;

Ø increasing the concentration of hydrogen ions in the interstitial environment.

An increase in the permeability of the vessels of the microvasculature leads to an increase in the passive transport of fluid through osmosis, ultrafiltration, diffusion, and active transfer through microvesiculation.

In some diseases of an infectious and non-infectious nature, the transmural transfer of blood cells increases: erythrocytes, platelets, leukocytes. The main reason is increased vascular permeability. The release of erythrocytes - diapedesis, is believed to be the result of their passive extrusion from the vessels through the interendothelial gaps under the influence of increased hydrodynamic pressure. Pathological processes such as inflammation, toxicosis, allergic reactions, ionizing radiation are accompanied by a significant increase in permeability and an increased exit of leukocytes, platelets, and erythrocytes outside the vessels. More gross damage to the integrity of the walls of the vessels of the microvasculature ends with microhemorrhages. One of the causes of erythrocyte diapedesis and microhemorrhages is thrombocytopenia. It is accompanied by dystrophic processes in endothelial cells, their death and, as a result, a sharp increase in permeability.

Extravascular, extravascular (from Latin exter - external, vas - vessel) microcirculation disorders are expressed in the fact that with increased extravasation, the outflow of interstitial fluid into the venous and lymphatic channels is difficult.

Difficulty in outflow with increased extravasation leads to accumulation of fluid in the tissues, the formation of edema.

The increased release of fluid into the interstitial space is due to an increase in hydrodynamic pressure on the walls of the arterial component of the microvasculature, a decrease in oncotic blood pressure (starvation, albuminuria, protein loss during burns, wound exhaustion, inhibition of the protein-forming function of the liver, etc.), an increase in colloid osmotic pressure in tissues due to the breakdown of large protein molecules into smaller ones, the accumulation of sodium ions.

Difficulty in reabsorption of fluid can be caused by an increase in hydrodynamic pressure in postcapillaries and venules (venous hyperemia), an increase in tissue colloid osmotic pressure, and narrowing of intercellular gaps.

In cases where the lymph nodes are not able to provide drainage to the interstitium, they speak of insufficiency of the lymphatic system. Consider the following forms:

ξ dynamic insufficiency, when the volume of interstitial fluid exceeds the ability of the lymphatic system to provide its outflow;

ξ mechanical failure occurs when the lymphatic vessels are squeezed from the outside (scars, tumors, edematous fluid), the formation of blood clots in their lumen, embolism, adynamia, which slows down the lymph flow;

ξ resorption deficiency is due to structural changes in the interstitial tissue.

Difficulty in the outflow of fluid, its accumulation in the interstitium are accompanied by an increase in the content of metabolic products, biologically active substances, ions in the tissues, which aggravates the severity of the pathological process.