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自60年代以来关于阿司匹林(ASA)对血栓栓塞性疾病的防治作用已进行了大量实验和临床研究,本文就其进展综述如下。一、作用机理血小板沉积和血栓形成是造成动脉粥样斑块及心肌缺血的重要因素。血小板内主要合成血栓素A_2(TXA_2)。TXA_2抑制腺苷酸环化酶,降低血小板内CAMP水平,使血小板聚集和释放,血管收缩。血管内皮主要形成前列腺环素(PGI_2),而PGI_2激活腺苷酸环化酶,抑制血小板聚集,舒张血管平滑肌。TXA_2和PGI_2在血小板和血管的相互拮抗作用可能是
A large number of experimental and clinical studies have been conducted on the prevention and treatment of aspirin (ASA) against thromboembolic diseases since the 1960s. The progress in this article is summarized as follows. First, the mechanism of action Platelet deposition and thrombosis is caused by atherosclerotic plaques and myocardial ischemia an important factor. The main synthesis of thromboxane A 2 (TXA 2) in platelets. TXA_2 inhibits adenylate cyclase, reduces platelet CAMP levels, platelet aggregation and release, vasoconstriction. Prostacyclin (PGI_2) is mainly formed in the vascular endothelium, while adenosine cyclase (PGI_2) is activated by PGI_2 to inhibit platelet aggregation and relax the vascular smooth muscle. The antagonistic effects of TXA_2 and PGI_2 on platelets and blood vessels may be