摘要
缺血预处理是指心肌反复多次短暂缺血/再灌注,对随后长时间心肌缺血/再灌注的一种保护.缺血预处理对心肌的保护机制十分复杂,一般公认为线粒体ATP敏感性钾通道(mitoKATP)是心肌缺血预处理保护机制的终末效应器之一.mitoKATP开放后可通过以下3条途径对抗心肌缺血损伤:减少线粒体膜Ca2+通道对Ca2+内流的驱动力,抑制Ca2+内流,减轻心肌细胞钙超载;保护线粒体呼吸链,减轻自由基释放引起的损伤;抑制线粒体转换孔开放,防止细胞色素C从线粒体释放,减少细胞凋亡.
Ischemic preconditioning refers to a mechanism whereby brief periods of ischemia - reperfusion render a tissue relatively resistant to the harmful effects of a subsequent prolonged period of ischemia. More and more studies are shown that mitochondrial ATP sensitive potassium channel plays an import role, acting as an end - effector, in these pathways. Activation of mitochondrial ATP sensitive potassium channel will reduce calcium influx through the mitochondrial calcium channel, then alleviate calcium overload; it can protect the mitochondrial respiratory chain, reduce free radical induced injury; it also inhibits the opening of mitochondrial permeability transition pore, decreases the cytochrome C released from mitochondria, and reduces apoptosis in ischemia hearts.
出处
《湖州师范学院学报》
2007年第2期119-122,共4页
Journal of Huzhou University
关键词
心肌缺血预处理
线粒体ATP敏感性钾通道
心肌保护
ischemia preconditioning
mitochondrial ATP sensitive potassium channel
role of mitochondrial ATP sensitive potassium channel in cardioprotection
