Why does microcirculation fail?
Microcirculation disorders are triggered by three main groups of causes. First, these are central and regional hemodynamics disorders (heart failure, ischemia, venous hyperemia). Second, direct damage to microvessel walls in atherosclerosis, vasculitis, or tumor growth. Third, changes in the properties of the blood itself—its hemoconcentration during dehydration, hemodilution, or the development of DIC syndrome.
The basic pathogenesis scenario looks like this: etiological factors increase the level of proaggregants, cations, and high-molecular-weight proteins in the blood. This inevitably leads to adhesion, aggregation, and agglutination of formed blood elements (erythrocytes, platelets, leukocytes). As a result, blood and lymph flow slows down until complete stoppage—stasis develops.
Intravascular disorders and the sludge phenomenon
The intravascular group includes slowing of blood flow, its turbulence, and pathological blood shunting. Excessive extracapillary flow poses a particular danger: during severe stress or catecholamine release (e.g., in pheochromocytoma), arterioles spasm, and blood bypasses via arteriolovenular shunts. The capillary network is shut down, and the tissue suffers from severe ischemia.
A striking example of intravascular pathology is the sludge phenomenon (Sludge). This is the separation of blood into liquid plasma and dense conglomerates of clumped cells. Sludge can act both as a primary cause of microcirculation disorders and as a secondary complication. The sludge mechanism relies on two factors:
- Chemical factor: release of proaggregants (thromboxane A2, ADP, catecholamines). They force cells to clump together, break down, and release new portions of active substances, closing the vicious circle.
- Electrostatic factor: normally, erythrocytes are negatively charged and repel each other. During tissue damage, potassium, calcium, and sodium cations enter the blood, "recharging" cell membranes, turning them into magnets for each other. Adhesion to the vessel wall is achieved through the fixation of protein micelles.
Transmural disorders
These disorders are associated with changes in the barrier function of microvessels.
Increased permeability occurs due to the development of acidosis (non-enzymatic hydrolysis of the basement membrane takes place), activation of hydrolases, and also due to the rounding of endothelial cells, which widens interendothelial clefts. Fluid rapidly leaves the vascular bed due to excessive activation of basic mechanisms: filtration, energy-dependent transcytosis, diffusion, and osmosis. The result is the exit of cells into tissues, microhemorrhages, and the formation of hemorrhagic exudate. A similar picture is characteristic of severe sepsis, plague, and measles.
Decreased permeability is observed with thickening and sclerosis of the walls, as well as with a deficiency of energy for intracellular transport. This blocks the escape of plasma and critically reduces leukocyte migration into the focus of damage.
Extravascular disorders and the finale of the process
Extravascular disorders are pathological changes in the volume of intercellular fluid. Its excess against the background of delayed outflow leads to edema (in inflammation, allergy, venous congestion).
A decrease in the volume of interstitial fluid (during hypohydration) is no less dangerous: it triggers a concentration mechanism. The concentration of toxic metabolic products, cytokines, and ions sharply increases in tissues. This disrupts the membrane potential of cells, worsens their damage, and blocks the transport of oxygen and carbon dioxide.
Long-term persistence of any of these forms leads to capillariotrophic insufficiency. This is a complex failure in which blood and lymph circulation stops, transcapillary transfer and metabolism cease. Tissues undergo severe dystrophies, and reparative processes are completely blocked.
Briefly: answers to topical questions
Which inflammatory mediators promote increased vascular permeability?
Increased vascular permeability is promoted by inflammation and allergy mediators:
- Histamine.
- Kinin system.
- Hydrolytic enzymes.
- Other biologically active substances.
Their action is associated with an increase in the permeability of the filtration barrier, including as a result of loosening of the basement membrane.
What types of blood stasis are distinguished in pathologial physiology?
Pathological physiology distinguishes two main types of blood stasis:
- Primary stasis — true or capillary, which occurs as a result of intracapillary aggregation of blood cells.
- Secondary stasis — symptomatic, which is additionally subdivided into two sub-types:
- Ischemic stasis — develops as a result of severe ischemia and a sharp slowdown in arterial blood inflow.
- Venous-congestive stasis — occurs as a result of venous hyperemia, a significant slowdown in outflow, and blood hemoconcentration.
What are the stages of erythrocyte aggregation and sludge syndrome development?
The development of sludge syndrome includes starting parallel processes and subsequent stages of formed element clumping.
- Parallel processes — cell activation with the release of proaggregants, electrostatic "recharging" of cells by an excess of cations, and deposition of protein micelles on cells.
- Conglomerate formation — clumping of formed blood elements together.
- Blood separation — separation of blood into plasma and formed cellular aggregates.
The three "C"s of microcirculation: Capillaries/vessels (wall damage), Cardiac (hemodynamic disturbance), Composition of blood (viscosity and sludge) — the three main causes of any disorders.
Class and exam questions
How does ischemic stasis differ from venous-congestive stasis?
Ischemic stasis occurs due to poor arterial blood inflow, which activates cells and causes their aggregation. Venous-congestive stasis is associated with hindered outflow, blood hemoconcentration, and hypoxic damage to formed elements.
How do cations cause blood cell aggregation?
Normally, blood cells have a negative surface charge and repel each other. An excess of cations is adsorbed on the membranes, neutralizes this charge or changes it to positive, allowing cells to approach and stick together.
What is juxtacapillary blood flow and why is it dangerous?
This is a pathological shunt of blood from arterioles directly into venules via shunts, bypassing the capillary network. As a result, the tissue does not receive oxygen and nutrients, leading to local ischemia.
What does rounding of endothelial cells lead to?
Rounding of endotheliocytes leads to the widening of interendothelial clefts and the formation of channels. This is one of the key mechanisms of the pathological increase in microvessel permeability for fluid and cells.
What else to study on this topic
- Mechanisms of increased vascular wall permeability (the role of acidosis and hydrolases)
- Pathogenesis of sludge syndrome: from cell activation to blood separation
- Types of fluid transport across the endothelium (filtration, transcytosis, diffusion, osmosis)
- The effect of hemoconcentration and hemodilution on blood rheological properties
- The role of proaggregants in microthrombus formation and positive feedback
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