目的　本研究旨在探讨内毒素休克时肝线粒体H+-ATP酶和脂质过氧化的改变。方法　成年健康Wistar大鼠 80只 ,随机分为内毒素注射前、内毒素注射后 1、3、5、8h组及其对照组 ;予各组相应时相点活杀取肝组织制备线粒体 ,测定线粒体H+-ATP酶、MDA及血浆MDA含量。离体实验采用正常鼠肝线粒体和不同剂量的氧自由基生成剂 (FeSO4 /VitC)共同孵育后 ,测量H+-ATP酶活性。结果　内毒素休克早期线粒体H+-ATP酶活性升高 ,3h时其酶活性升高 15 6 % ,8h时降至对照组的 6 5 %。内毒素休克早期肝线粒体MDA含量就显著增高 ,随着休克时间延长而加重 ,8h时为对照组的 1 79倍。离体实验显示 ,小剂量FeSO4 /VitC引起的H+-ATP酶活性升高 ,大剂量引起H+-ATP酶活性下降 ,和在体实验结果平行。结论　内毒素休克早期H+-ATP酶升高 ,晚期H+-ATP酶活性降低。内毒素休克时脂质过氧化物进行性增加 ,脂质过氧化可能是H+-ATP酶下降的重要原因 Objective This study aimed to investigate changes of hepatic mitochondrial H + -ATPase and lipid peroxidation during endotoxic shock. Methods Eighty adult Wistar rats were randomly divided into three groups: control group, LPS group, control group, LPS group, Mitochondrial H + -ATPase, MDA and plasma MDA content. In vitro experiments using normal rat liver mitochondria and different doses of oxygen free radical generating agent (FeSO4 / VitC) co-incubated after measuring H + -ATPase activity. Results At early stage of endotoxic shock, mitochondrial H + -ATPase activity increased, 15 h at 3h, and 6 5% at 8h. Early liver endotoxic shock mitochondrial MDA content was significantly increased with the extension of shock time and aggravate, 8h when the control group was 79 times. In vitro experiments showed that low dose of FeSO4 / VitC caused by H + -ATPase activity increased, high dose caused H + -ATPase activity decreased, and in vivo experimental results parallel. Conclusions Endotoxin shock increased H + -ATP enzyme in the early stage and late H + -ATPase activity decreased. Endotoxic shock increased lipid peroxides, lipid peroxidation may be H + -ATP enzyme decreased the important reason