4. TYPICAL FORMS OF DISORDERS OF REGIONAL CIRCULATION AND MICROCIRCULATION

Typical forms of disorders of regional circulation include disorders of circulation in the medium size vessels and in microvessels. Typical disorders or regional circulation are presented in fig. 4.

Fig. 4

Arterial hyperemia is characterized by a local deposition of the blood and an increased blood flow rate through the organ or tissue resulting from a dilation of arterial vessels. Pathological arterial hyperemia, compared physiological one, does not correspond to metabolic demands of the organ or tissue.

Mechanisms of arterial hyperemia:

•  neurogenous mechanism - a decrease in the sympathetic drive;

•  humoral mechanism - local accumulation of vasodilator substances: kinins, histamine, prostaglandins, leukotrienes, nitric oxide, adenosine, hydrogen and potassium ions, carbon dioxide;

•  neuromyoparalytic - atrophy of sympathetic fibers and vessel smooth muscles following a prolonged compression of organs or tissues.

Manifestations and their mechanisms:

•  redness - reduction of deoxygenated hemoglobin in the capillaries and venules;

•  an increased temperature - an increased inflow of the warm blood from the body core;

•  vessel pulsation;

•  slight swelling - mild accumulation of fluid in the interstitial space resulted from an increase in filtration rate;

•  an increased number of functioning capillaries - opening of precapillary sphincters;

•  an increased lymphatic outflow - mild elevation of interstitial hydrostatic pressure.

The most common form of arterial hyperemia seen clinically is reactive hyperemia.

Reactive hyperemia is due to humoral and myoparalytic mechanisms. When the blood supply to tissue is blocked and then is unblocked, the flow through the tissue can increase to about five times normal. The duration of reactive hyperemia corresponds to the duration of the ischemic period. Reactive hyperemia may exert harmful effects that result from increased production of free oxygen radicals with the following membrane damage and an impairment of intracellular calcium exchange. Moreover accumulation of the blood during arterial hyperemia increases intracranial pressure that may cause a reduction of the cerebral blood flow and brain mass displacement.

Venous hyperemia is characterized by a local deposition of the blood and a decrease in the blood flow rate through the organ or tissue resulting from a reduction or cessation of the blood outflow via the venous vessels.