缺血预适应的研究现状和前景

Ischemic preconditioning: present situation and future prospects

缺血预适应是一种内源性保护机理 ,即短暂缺血后能耐受随后较长时间的缺血损伤 ,这一现象已在不同种属动物和临床病人中得到证实 .缺血预适应表现为早期和延迟心肌保护 .缺血预适应的信号转导途径涉及触发物质 (内源性活性物质 ) ,中介物质 (蛋白激酶 )和效应物质 (离子通道和保护蛋白 ) .核因子 - κB可能在心肌缺血预适应的延迟保护中起重要作用 .缺血预适应已扩展到药理性预适应 ,单磷酯 A,尼可地尔等能显著减轻心肌缺血损伤 .

Ischemic preconditioning is an endogenous protective mechanism in which brief periods of myocardial ischemia and reperfusion render the myocardium resistant to a subsequent more sustained ischemic insult. This phenomenon has been confirmed in a variety of animals and in humans. Transient ischemia (preconditioning stimulus) not only triggers early preconditioning, but also induces delayed protection. The signal transduction pathways of ischemic preconditioning involve triggers (endogenous active substances), mediators (protein kinases) and effectors (ionic channels and protective proteins). Nuclear factor κB may play an essential role in the late phase of ischemic preconditioning. The cardioprotection of preconditioning was extended from ischemic stress to pharmacological preconditioning, and it has been shown that monophosphoryl lipid A and nicorandil significantly reduce myocardial injury due to ischemia reperfusion.