下肢動脈の動脈硬化の形態, 成立ち, 血栓形成の機序について

Abstract

Morphogenesis of atherosclerosis and vascular lesions as the cause of thrombus formation in the arteries of the lower limb were investigated histologically and immunohistochemically.Fibrocellular intimal thickening of the arteries in the newborn was localized in bifurcaitons of the femoral artery and slightly involved non-bifurcated segments of the artery within two years. The pronounced and laminated intimal thickening which was frequently observed in hypertensives resulted from repeated proliferation or growth of the intimal tissue. It seems probable that various kinds of stimuli repeatedly affect on the arterial wall leading to make a reactive or regenerative proliferation of the intimal cells and endothelial cells.Infiltration of plasma constituents into the intima as slight as being not able to detect until using with an immunohistochemical method was diffusely observed in the fibrocellularly thickened intima.There were preferential sites where severe infiltration of blood plasma lipids and proteins into the intima occurred. Appearances with blood plasma, extracellular lipid and foam cells were sometimes seen at edge of the thickened intima and in the interlayer junctions between formerly and newly established layer of the intima. Markedly enhanced permeability in these special sites may be drove by two kinds of forces. One is a force splitting junctions between the thickened intima and media and also between each intimal layer, due to contraction of smooth muscle cells which are running in different directions in each layer of the arterial wall. The others are hemodynamic factors, i. e. turbulence of blood stream and increased tensil force occurring on shoulder of the thickend intima. These forces affect on the endothelial cells and injure them.In the femoral and popliteal arteries thrombi were formed on segments involved with severe atherosclerosis and with accumulation of many foam cells beneath the endothelium. Thrombosis in the peripheral arteries below the knee was found on the intima showing fibrocellular thickening or edema. In the proximal arteries tear or split of superficial layer in the atherosclerotic intima plays an important role in thrombogenesis. There are many various causes of the tear being able to be considered, for instance, 1) a large tensil force acting on shoulder of the thickened intima, 2) structural discontinuity at abutting areas between different layers of arterial wall, and 3) histolytic effects of foam cells and the blood plasma accumulated in the intima, presumably effects of some unknown active substances derived from foam cells or contained in the blood plasma.