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局部缺血部位快速再灌注虽然保护了心肌,但也引起再灌注损伤。目前还没有减轻再灌注损伤的特效疗法,但近年来研究显示,G蛋白耦联受体(G protein-coupled receptor, GPCR)的激动剂、胰岛素和缺血后处理可以在各种实验条件和各类动物模型中有效抵抗再灌注损伤。这些干预手段启动的心脏保护机制可能包括激活再灌注损伤补救激酶(reperfusion injurysalvage kinase, RISK)途径、抑制糖原合酶激酶-3β(glycogen synthase kinase 3β, GSK-3β)以及抑制线粒体膜通透性转换孔(mitochondrial permeability transition pore, mPTP)开放等。这些研究成果有利于开发治疗急性心肌梗死的有效临床手段。
Rapid reperfusion at the ischemic site protects the myocardium but also causes reperfusion injury. At present, there are no specific therapies for reducing reperfusion injury. However, recent studies have shown that G protein-coupled receptor (GPCR) agonists, insulin and ischemic postconditioning can be used under various experimental conditions and Animal models effectively resist reperfusion injury. Cardiac protection mechanisms initiated by these interventions may include activating the reperfusion injurysalvage kinase (RISK) pathway, inhibiting glycogen synthase kinase 3β (GSK-3β), and inhibiting mitochondrial membrane permeability The opening of mitochondrial permeability transition pore (mPTP) and so on. These findings are conducive to the development of effective clinical treatment of acute myocardial infarction.