肉苁蓉对感染性休克大鼠肝线粒体ATP酶影响的实验研究

目的：研究肉苁蓉对感染性休克肝线粒体ATP酶的影响．明确肉苁蓉治疗感染性休克的机制．方法：40只SD大鼠随机分为五组：假手术组；12小时对照组；12小时给药组；16小时对照组；16小时给药组。采用盲肠结扎穿孔术（CLP）复制败血症模型，比较各组存活率和平均动脉压（MAP），肝线粒体ATP酶活性的变化。结果：大鼠在复制感染性休克模型后，肝线粒体ATP酶活性降低，24小时存活率明显下降。给予肉苁蓉后肝线粒体ATP酶活性较对照组明显改善（P〈0.05）。与大鼠死亡率的降低呈显著正相关。结论：感染性休克线粒体ATP酶活性下降，细胞钙超载和水肿坏死是败血症大鼠死亡的直接原因，肉苁蓉能增强ATP酶活性是肉丛蓉治疗感染性休克的重要机制。

Effective of Cistanche deserticola Y.C.Ma to rats hepatocytic mitochondrial ATPase following septic shock

Objective： To study effective of Cistanche deserticola Y.C.Ma to rats liver mitochondrial ATPase following septic shock. Methods： 40 rats were randomly divided into 5 groups： artificial groups; 12h control groups; 12h Cistanche deserticola Y.C.Ma groups; 16h control groups; 16h Cistanche deserticola Y.C.Ma groups.The model of septic shock was made by cecal ligation and puncture.Cistanche deserticola Y.C.Ma and saline were via gastric garage to the rats respectively for fifteen days.Liver mitoehondrial ATPase activity and rats dead of rate were assayed.Results： Rats liver mitochondria ATPase activity were obviously decreased following CLP.After give Cistanche deserticola Y.C.Ma, mitochondria ATPase activity was significantly better than control group （P〈 0.01）, Furthermore keep positive correlation with improvement of dead of rate.Conclusion： Mitochondrial ATPase activity decreased,, cellulate Ca^2＋ over loading and dropsy and necrosis.That＇s the death cause of rats following septic shock.Cistanche deserticola Y.C.Ma can strengthen mitochondrial ATPase activity.