缺血时线粒体氧化磷酸化不能有效进行 ,ATP生成减少而水解增多 ,细胞因能量不足发生功能障碍。随着缺血时间延长 ,线粒体结构和功能受损 ,ATP耗竭 ,细胞功能进一步损害 ,甚至发生细胞凋亡。再灌注时线粒体产生大量氧自由基 ,同时线粒体钙转运紊乱 ,发生永久性通透性转换 ,胞浆钙浓度急剧升高 ,导致细胞坏死。 Ischemia mitochondrial oxidative phosphorylation can not be effectively carried out, ATP production decreased hydrolysis increased, lack of energy due to cell dysfunction. With prolonged ischemia, mitochondrial structure and function of damaged, ATP depletion, cell function further damage, and even apoptosis. During reperfusion, mitochondria produce a large amount of oxygen free radicals. At the same time, mitochondrial calcium transport disorder, permanent permseal conversion, cytoplasmic calcium concentration increased dramatically, leading to cell necrosis.