论文部分内容阅读
近来,随着溶栓和介入治疗的发展,AMI再灌注成功率显著提高。但是,血管再通时随之可能会发生缺血心肌的再灌注损伤。已证实缺血预处理(IPC)可产生心肌保护作用。而阿片受体激动剂通过激活心肌阿片受体能模拟缺血预处理对心脏的保护作用,心肌阿片受体激活能产生早期时相和后时相的心肌保护作用,信号途径涉及Gi/Go、蛋白激酶C、酪氨酸激酶和ATP敏感钾离子通道等。另外,阿片受体激动药对缺血/再灌注心肌也可产生直接的保护作用。但其作用机制有待于进一步的研究。
Recently, with the development of thrombolysis and interventional therapy, the success rate of AMI reperfusion was significantly increased. However, reperfusion may lead to reperfusion injury of ischemic myocardium. It has been demonstrated that ischemic preconditioning (IPC) produces cardioprotection. The opioid receptor agonist can activate cardiomyocyte opioid receptor to mimic the protective effect of ischemic preconditioning on the heart. Myocardial opioid receptor activation can induce cardioprotection in early phase and in posterior phase. The signaling pathway involves Gi / Go, Protein kinase C, tyrosine kinase and ATP-sensitive potassium channel. In addition, opioid agonist drugs can also have a direct protective effect on ischemia / reperfusion myocardium. However, its mechanism remains to be further studied.