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血栓形成在心脏梗塞中的作用是早已确定的。绝大多数有梗塞证据的病人尸检在冠脉中均有血栓,而梗塞后生存者进行血管造影有很高比率证明有阻塞,大多由于血栓所致。另一方面,猝死者仅有小部分病人可发现阻塞性血栓。然而,因心律失常致猝死可在动物中因血小板凝集堵塞冠脉微循环而引起,因而提示血小板在猝死中起关键作用:或因凝集而堵塞微循环血管,或由血小板释放血栓恶烷A_2(TxA_2)引起血管痉挛。一、阿司匹林的抗血栓形成作用上述结果引起了对血小板凝集的强力抑制剂—阿司匹林的兴趣。阿司匹林有两种与血栓形成有关的作用:①可抑制血小板血栓恶烷A_2的合成,因而减少凝集。②可抑制血管壁中前列环素(PGI_2)的合成。PGI_2本身可抑制血小板凝集及促进平滑肌松弛。因
The role of thrombosis in heart infarction has long been established. The vast majority of patients with evidence of infarction had an autopsy with thrombi in the coronary arteries, and a high rate of angiography in the survivors of the infarction proved obstructive, mostly due to thrombus. On the other hand, only a small percentage of sudden death patients can find obstructive thrombi. However, sudden death due to arrhythmia can be caused by blockage of coronary microcirculation by platelet aggregation in animals, suggesting that platelets play a key role in sudden death: blockage of microcirculation by agglutination or release of thromboxane A2 TxA_2) causes vasospasm. First, the antithrombotic effect of aspirin The above results caused a strong inhibitor of platelet aggregation - aspirin interest. There are two effects of aspirin and thrombosis: ① can inhibit the synthesis of platelet thromboxane A_2, thus reducing the agglutination. ② inhibit the synthesis of prostacyclin (PGI_2) in the vascular wall. PGI_2 itself inhibits platelet aggregation and promotes smooth muscle relaxation. because