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[Effects of exogenous cholesterol on the functional morphology of blood formed elements in atherogenesis dynamics].

Results of clinical and experimental studies showed that exogenous cholesterol is a factor of initiation of athero- and thrombogenesis that under conditions of failure of compensatory reactions are manifested by generation and progression of illness. In the control group of observation, activation of leukocytes in indicative of reciprocal reactions of cell-bound immunity directed to elimination of atherogenic lipoproteids whereas in patients with ischemic heart disease, the cholesterol load apparently provokes cell type effector reactions leading to damage to and necrosis of cells. In healthy subjects, chemotaxis and phagocytosis become activated while in sick persons they get supressed. We can well believe that there takes place fixation of an antigen (in the given case--apo-beta lipoproteins) on macrophages and polymorphonuclear leukocytes with subsequent cascade to follow such as activation of lipooxygenase, active forms of oxygen, superoxydes, cytokins, as well as production of elastase and collagenase, which fact in the presence of a high degree inter-cellular cooperation results in formation of a vicious circle. The findings secured corraborate etiological significance of exogenous cholesterol and saturated fatty acids as a starting-point of atherogenesis.