The late reperfusion of AMI promotes the expression of Fas/FasL and myocardial apoptosis,and it may be due to oxidative stress mechanism.

• AM I晚期再灌注使梗死边缘区心肌细胞Fas/FasL蛋白表达以及细胞凋亡指数增加,提示晚期再灌注仍然存在再灌注损伤,其机制可能与氧化应激有关。