摘要
再灌注治疗是急性心肌梗死的重要治疗手段,再灌注治疗在迅速恢复缺血心肌的血液灌注,挽救大量濒死心肌的同时也引起再灌注损伤。近年来大量实验研究及临床应用表明,后适应可以减轻再灌注损伤,其信号转导通路虽未完全阐明,但抑制再灌注早期线粒体mPTP开放,减轻mPTP开放引起的细胞坏死被认为是其作用的重要原因。
After an acute myocardial infarction,early reperfusion remains the most effective strategy for rapid recovery of blood perfusion in ischemic myocardium and saving a large number of dying myocardial. However,lethal reperfusion injury can not be ignored. Nowadays, many researches conclude that post-conditioning can reduce the injury. Postconditioning have been successfully applied to the clinical setting and have been found to reduce infarct size. The signal pathways are incompletely mapped but they probably converge on suppression of mPTP （mitochondrial permeability transition pore） opening during early reperfusion, an event that is thought to promote cell death at reperfusion. In this article, the protection mechanism of myocardial ischemic postconditioning were reviewed.
出处
《医学综述》
2010年第3期413-416,共4页
Medical Recapitulate
关键词
缺血后适应
心肌
再灌注损伤
Ischemic postconditioning
Myocardium
reperfusion injury
