论文部分内容阅读
目的研究内毒素、失血性休克大鼠肝线粒体质子跨膜转运和Ｈ＋－ＡＴＰ酶的变化。方法大肠杆菌内毒素休克模型和失血性休克模型。采用荧光探针ＡＣＭＡ测定质子跨膜转运。结果（１）内毒素休克５小时亚线粒体在以ＡＴＰ、ＮＡＤＨ和ｓｕｃｃｉｎａｔｅ为底物时引起的ＡＣＭＡ最大荧光淬灭值显著减少（Ｐ＜０．０５）；最大荧光淬灭时间和半数荧光淬灭时间非常显著延长（Ｐ＜０．０１）。（２）内毒素休克早期，线粒体Ｈ＋－ＡＴＰ酶活性显著升高（Ｐ＜０．０５），晚期非常显著下降。（３）内毒素休克大鼠肝线粒体膜结合ＰＬＡ２、血浆和线粒体ＭＤＡ升高（Ｐ＜０．０５）。（４）失血性休克时Ｈ＋－ＡＴＰ酶和质子转运无显著改变。结论内毒素休克时线粒体跨膜质子转运和Ｈ＋－ＡＴＰ酶活性显著下降，失血性休克时变化不大
Objective To study the changes of proton transmembrane transport and H + -ATPase in hepatic mitochondria of endotoxin and hemorrhagic shock rats. Methods E. coli endotoxin shock model and hemorrhagic shock model. Proton transmembrane transport was measured by fluorescent probe ACMA. Results (1) The maximum fluorescence quenching value of ACMA induced by ATP, NADH and succinate in sub mitochondria after endotoxin shock for 5 hours was significantly decreased (P <0.05). The maximum fluorescence quenching time and half fluorescence quenching The time was significantly longer (P <0.01). (2) At the early stage of endotoxic shock, mitochondrial H + -ATPase activity was significantly increased (P <0.05), and the late phase was significantly decreased. (3) LPS-induced mitochondrial membrane-bound PLA2 in endotoxic shock rats increased in plasma and mitochondria (P <0.05). (4) H + -ATPase and proton transport did not change significantly in hemorrhagic shock. Conclusions Endotoxin shock mitochondrial membrane transmembrane proton transport and H + -ATPase activity decreased significantly, hemorrhagic shock did not change much