Przyklenk K, Kloner R A
Heart Institute, Good Samaritan Hospital and Department of Medicine, University of Southern California, Los Angeles 90017-2395, USA.
Prog Cardiovasc Dis. 1998 May-Jun;40(6):517-47. doi: 10.1016/s0033-0620(98)80002-9.
Brief transient episodes of nonlethal myocardial ischemia protect or "precondition" the heart and render the myocardium resistant to a subsequent more sustained ischemic insult. The hallmark of this phenomenon--documented in virtually all species and experimental models evaluated to date in countless laboratories worldwide--is the profound reduction in infarct size seen in preconditioned groups versus time-matched controls. Efforts to identify the cellular mechanisms responsible for this paradoxical ischemia-induced cardioprotection, to expand the definition of ischemic preconditioning beyond infarct size reduction, and, perhaps most importantly, to evaluate the efficacy of preconditioning in disease models and in the clinical setting, are all topics of intensive ongoing investigation.
短暂的非致死性心肌缺血发作可保护心脏或使其“预处理”，从而使心肌对随后更持久的缺血损伤具有抵抗力。这一现象的标志——在全球无数实验室迄今评估的几乎所有物种和实验模型中都得到了证实——是预处理组与时间匹配的对照组相比，梗死面积显著减小。确定导致这种矛盾的缺血诱导心脏保护作用的细胞机制、将缺血预处理的定义扩展到梗死面积减小之外，以及或许最重要的是，评估预处理在疾病模型和临床环境中的疗效，都是正在深入研究的课题。
