[Participation of monocytes in the pathogenesis of peripheral arterial obliterating disease]

The damage of the vascular endothelial cells is considered as the primary factor of the development of atherosclerotic changes. The damaged vascular endothelial cells secrete lower amounts of tissue plasminogen activator, antithrombin III, thrombomodulin, endothelium devived relaxing factor (EDRF) prostacycline (PGI2) and glycosaminoglycans. An increase of plasma viscosity and blood procoagulation activity is observed in the peripheral arterial obliterative disease as a result of the interaction between platelets, leucocytes and erythrocytes from the walls of the damaged vessels together with the impairment of blood fibrinolytic activity. It is considered that one of the factors responsible for the development of the atherosclerotic changes is chronic inflammation process of the vascular endothelium. This causes a considerable participation of inflammation cells, i.e. lymphocytes and monocytes in atherosclerosis development. It is observed that an increased level of tissue factor (TF) and factor VII produced as a result of their releasing by the activated monocytes in the atheromatous lamina rupture exerts procoagulation effect. The tissue factor inhibitor inhibits VIIa/TF/Xa complex activity.