5. 動脈硬化と凝固・線溶・血小板

抄録

Many of reports showed an enhancement of blood coagulability, a decrease in fibrinolytic activity and an enhancement of platelet function in arteriosclerotic diseases. However, there were several discrepancies in the above results. we have found an enhancement of platelet aggregation associated with a consumption of larger platelets which are known to have hyperfunction in arteriosclerotic patients. The circulating platelets in these patients contained less amount of ADP compared to those collected from healthy control. The plasma thromboxane B₂ and 6-keto-PGF₁α levels and the platelet TXA₂-synthetizing activity of the arteriosclerotic patients were similar to those collected from the healthy control. In the acute stage of myocardial infarction, TXA₂-synthetizing activity of platelets showed a marked decrease. The results suggest that platelets in the arteriosclerotic diseases were activated by the presense of injured surfaces of blood vessels and the activated platelets were consumed selectively in the circulation. On the one hand, platelet sensitivity to ADP aggregation, plasma von Willebrand factor and plasma β-thromboglobulin increased significantly after an isometric exercise in the arteriosclerotic patients. The changes were prevented by a pretreatment of anti-platelet drugs. The isometric exercise may induce platelet activation accompanied with release reaction in vivo through an interaction with arteriosclerotic lesions in blood vessels and may produce a thrombogenic tendency in the arteriosclerotic diseases. The changes in platelets may play an important role in atherogenesis also.