乌司他丁在肝脏缺血再灌注损伤中的作用

Protective effects of ulinastatin on mitochondrial function of hepatic ischemia-reperfusion injury

目的探讨乌司他丁在肝脏缺血再灌注损伤中对线粒体的作用。方法采用健康杂交狗全肝缺血再灌注模型,检测肝功能、线粒体Na+-K+-ATP酶活性及电镜观察线粒体形态的变化。结果实验组缺血15min后Na+-K+-ATP酶活性为0.128±0.012,而对照组为0.089±0.011(P<0.05);再灌注1h后实验组Na+-K+-ATP酶活性为0.121±0.011,对照组为0.092±0.025(P<0.05)。实验组线粒体结构损伤较对照组明显减轻。结论乌司他丁在肝脏缺血再灌注损伤中对线粒体有明显保护作用,其机制是稳定线粒体膜结构及增强线粒体Na+-K+-ATP酶活性。

Objective To study the protective effects of ulinastatin on mitochondrial function during ischemiareperfusion of liver. Methods Based on the model of total hepatic I/R injury in dog. The hepatic function and the activity of Na^＋-K^＋-ATPa were determined. The ultrastructure of mitochondria was observed by electron microscope. Results The activity of Na^＋-K^＋-ATPase was 0. 128± 0. 012 in experiment group and 0. 089±0. 011 in control group after 30 minutes of ischemia （P 〈 0.05）. It was 0. 121 ±0. 011 in experiment group and 0. 092 ± 0. 025 in control group after 60 minutes of ischemia （ P 〈 0.05）. The damage of mitochondrial uhrastructure in experiment group was significantly lower compared with control group. Conclusion Ulinastatin has protective effects on mitochondrial function of hepatic ischemia-refusion injury. The mechanism is to stabilize mitochondrial membrane structure and to improve activity ofNa^＋-K^＋-ATPase.