Hua J D
First Affiliated Hospital, Second Military Medical College, Shanghai.
Zhonghua Wai Ke Za Zhi. 1992 Nov;29(12):774-6, 799.
We observed the alterations in mitochondrial function and activity of endogenous SOD, and studied the protective effects of SOD on rats with hemorrhagic shock. It was found that after two hours' shock, RCR in hepatic and kidney mitochondria decreased significantly (liver P less than 0.01, kidney P less than 0.05), the activity of endogenous SOD depressed more or less in samples of blood and mitochondrial fraction (blood P less than 0.01. liver P less than 0.01. kidney P greater than 0.05). Further descent was found in these parameters in the deteriorating process of shock. After the rats were treated with SOD, RCR and activity of endogenous SOD increased considerably. Mere reflow did not affect them remarkably. This results suggest that oxygen-derived free radicals be the important factor impairing mitochondrial function in hemorrhagic shock, and that SOD can effectively ameliorate mitochondrial function.
我们观察了线粒体功能及内源性超氧化物歧化酶(SOD)活性的变化,并研究了SOD对失血性休克大鼠的保护作用。结果发现,休克两小时后,肝和肾线粒体的呼吸控制率(RCR)显著降低(肝脏P<0.01,肾脏P<0.05),血液及线粒体部分样本中的内源性SOD活性或多或少有所降低(血液P<0.01,肝脏P<0.01,肾脏P>0.05)。在休克恶化过程中,这些参数进一步下降。用SOD治疗大鼠后,RCR和内源性SOD活性显著增加。单纯再灌注对其影响不明显。这些结果表明,氧自由基是失血性休克中线粒体功能受损的重要因素,且SOD可有效改善线粒体功能。