摘要
缺血后处理(ischemic postconditioning)是在长时间缺血后再灌注早期,对心脏进行数次短暂的再灌注/缺血处理的方法。研究表明,缺血后处理与预处理一样能减轻再灌注心肌的损伤。其保护心肌的作用可能与抑制自由基生成、减轻钙超载、激活蛋白激酶、内源性生成物(如腺苷、阿片肽、一氧化氮等)激活、线粒体的ATP敏感性钾通道开放和线粒体通道转换孔关闭有关。现就后处理对心肌缺血再灌注的保护作用及其机制作一简要综述。
Postconditioning is defined as rapid intermittent periods of reperfusion and ischemia in the early phase of reperfusion after long ischemia. It has been found that ischemic postconditioning can reduce myocardial ischemia-reperfusion injury just as ischemic preconditioning. Mechanisms using postconditioning have been associated with a reduction in the generation of superoxide radicals and calcium overload, activation of protein kinases, preservation of endogenous autacoids （ such as adenosine, opioids, and NO ） , opening of mitochondrial ATP-sensitive potassium channels and closing of mitochondrial transition permeability pore. This article summarizes the current information regarding the cardioprotection of postconditioning in ischemia-reperfusion and possible mechanisms involved.
出处
《心血管病学进展》
CAS
2007年第6期917-920,共4页
Advances in Cardiovascular Diseases
关键词
缺血后处理
缺血再灌注
心肌保护
ischemic postconditioning
ischemia-reperfusion
cardioprotection
