[Microcirculatory changes in chronic venous insufficiency].

Abstract

INTRODUCTION: The venous system of lower leg can be topographically divided into two subsystems: superficial (extrafascial) and profound (subfascial). Functionally, we can divide circulation in to macrocirculation (arteries and veins) and microcirculation (arterioles, capillaries, and venules). Blood flow towards heart can be disturbed by different pathological conditions, and than chronic venous insufficiency (CVI) develops. First alterations occurs in macrocirculation, and after some period changes in microcirculation also appear. Those changes are leading to the ultimate stage in CVI--venous ulcer. RESULTS AND DISCUSSION: Previous conceptions that alterations in microcirculation in CVI are consequences of venous stasis, high pressure in capillaries and anoxic tissue are still actual. Observations that partial pressure of oxygen is higher in venous blood of lower limbs with ulceration than in limbs without ulceration lead to hypothesis that blood is passing directly from arterioles to venules over arterio-venous temperature-regulating shunts in dermis. Histological and electron-microscopic examinations certain alterations in the structure of capillaries. Raised pressure in these altered capillaries leads to exudation of plasma and fibrinogen in the interstitial space. Soluble fibrinogen is transformed to insoluble fibrin and forms fibrin cuffs. These cuffs are a barrier for normal diffusion of oxygen. Recently, it was observed that blood cells can adhere to the endothelial cells--Leukocyte trapping hypothesis. It can be explained by slower blood flow velocity and also by expression of certain endothelial and leukocyte adhesion molecules intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1). This causes congestion of white blood cells which leads to tissue damage due to secretion of inflammatory mediators.