缺血后处理内源性心脏保护的研究进展

Progress in endogenous cardioprotection induced by ischemic postconditioning

再灌注疗法是临床治疗心肌缺血最有效的措施,但会引起再灌注损伤,调动机体内源性保护机制可以减轻再灌注损伤,保护缺血心肌。缺血预处理(ischemic preconditioning,IPC)和后处理(ischemic postconditioning,I-postC)是缺血心脏有效的内源性保护现象,可以减轻缺血再灌注(ischemia/reperfusion,I/R)后心肌坏死与心肌功能障碍,减少恶性心律失常的发生。内源性心脏保护的机制主要是通过诱导触发因子释放,经多条细胞内信号转导途径的介导,作用于多种效应器,影响氧自由基产生、钙超载等I/R损伤的关键环节而发挥心肌细胞保护作用。特别是可以在缺血后实施的I-postC具有良好的临床应用前景。本文以I-postC为重点综述内源性心脏保护作用、机制及其临床应用现状。

Restoration of blood flow is the definitive therapy to salvage myocardium following ischemic injury. Sudden restoration of blood flow to the ischemic myocardium may, however, also cause reperfusion injury. Therefore, to prevent such ischemia/reperfusion （I/R） injury, one strategy could be to evoke endogenous myocardial protective mechanisms. Ischemic preconditioning （IPC） and postconditioning （I-postC） are endogenous protective mechanisms capable of protecting the myocardium from myocardial infarction, stunning, and ventricular arrhythmia induced by I/R injury. The mechanisms involve induction of triggers, activation of signaling pathways, and end-effectors, which attenuate generation of free radicals and calcium overload induced by I/R. The fact that I-postC can be applied after a prolonged period of ischemia offers a novel approach to myocardial protection. This article mainly reviews the cardioprotection, mechanisms, and application to clinical cardiology of I-postC.