Hyperemia

Mechanisms of redness (Rubor)

A classic sign of inflammation — redness of the skin or mucous membranes — is caused by the development of arterial hyperemia. This process affects several links of the microvasculature at once:

• There is a notable increase in the number of functioning precapillaries and their pronounced dilation.
• The number of capillaries in the tissue increases, and they actively fill with incoming arterial blood.
• So-called arterialization of venous blood occurs. Due to the high blood flow velocity, tissues do not have time to fully utilize oxygen. As a result, blood with an abnormally high oxyhemoglobin ($HbO_2$) content enters the venous bed, giving the affected area its characteristic bright color.

Venous hyperemia and development of edema

While arterial hyperemia is associated with inflow, venous hyperemia is related to hindered outflow from the tissue. The main consequence of venous hyperemia is hydrodynamic edema.

The pathogenesis of this condition at the level of an individual capillary is as follows:

1. Hemodynamic pressure rises sharply in the venous section of the capillary bed.
2. Consequently, the gradient (difference) between hemodynamic pressure and plasma colloid-osmotic pressure drops.
3. The rate of fluid return (reabsorption) from the intercellular space back into the vessel decreases significantly.
4. Unremoved fluid begins to accumulate in the interstitium, forming edema.

Important nuance: at the same time, the rate of plasma filtration at the arterial end of the capillary remains unchanged. Fluid accumulation increases hydrostatic pressure in the interstitium, which triggers a compensatory reaction — the tissue tries to get rid of fluid through enhanced lymph formation and accelerated lymphatic drainage.

Sequence of microcirculatory changes

Circulatory disorders in the affected area do not develop instantaneously, but go through a strict sequence of stages:

1. Short-term ischemia. Serves as the starting reaction. Smooth muscle cells of arterioles and precapillaries increase their tone, vessel lumens narrow (vasoconstriction), leading to a temporary decrease in blood flow.
2. Arterial hyperemia. Smooth muscle tone of arterioles drops. Vessels dilate, and tissue becomes abundantly filled with arterial blood. Concurrently, lymph formation and outflow processes are enhanced.
3. Venous hyperemia and lymphostasis. Develops after several tens of minutes. The lumens of venules and lymphatic vessels decrease (due to narrowing or external compression). Blood and lymph outflow is impaired.
4. Stasis and sludge phenomenon. Vascular tone at all levels changes in a dyscoordinated manner. The rheological properties of blood change: formed elements begin to actively adhere to the walls (adhesion), stick together (aggregation and agglutination). Blood thickens, a sludge forms, and blood flow stops completely (stasis).

Prolonged persistence of stasis deprives the tissue of nutrition, inevitably leading to dystrophic changes and death (necrosis) of the affected areas.

Class and exam questions

What else to study on this topic

• Mechanisms of changes in blood rheology during the sludge phenomenon
• Compensatory mechanisms of lymph formation in hydrodynamic edema
• Pathogenesis of venous blood arterialization: tissue oxygen balance
• Dyscoordination of vascular tone in terminal stages of microcirculatory disorders
• Tissue dystrophy and necrosis as a consequence of prolonged stasis

Other topics in section "Chapter 5. The Inflammatory Process"

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