乌司他丁在肝脏缺血再灌注损伤中的作用

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。

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

Objective To study the protective effects of ulinastatin on mitochondrial function during ischemia-reperfusion of liver.Methods Based on the model of total hepatic I/R injury in dog.The hepatic function and the activity of Na+-K+-ATPase 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 ultrastructure 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 of Na+-K+-ATPase.