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目的对不同条件下骨骼肌线粒体RCR(呼吸控制率)的测定水平评估缺血再灌注对线粒体活性的影响。方法通过夹闭大白鼠右髂总动脉,造成骨骼肌缺血再灌注损伤的模型,并对不同缺血时期及再灌注或右股静脉静注NSMA(3-硝基-N-甲基水杨酰胺)再灌注后的腓肠肌提取线粒体进行RCR测定。结果2,3,5,6组与对照组相比RCR下降(P<0.01),差异具有非常显著性意义;4组与对照组比RCR无明显变化(P>0.05),7组与对照比RCR下降(P<0.05),差异具有显著性意义。各用药均比相对应组线粒体RCR明显提高。结论在缺血再灌注后,线粒体活性显著降低,氧化磷酸化偶联程度下降;研究提示NSMA可能影响呼吸链电子传递,使氧自由基产生减少,从而改善骨骼肌缺血再灌注时线粒体的活性。
Objective To evaluate the mitochondrial activity of mitochondria induced by ischemia-reperfusion in skeletal muscle mitochondrial RCR (respiratory control rate) under different conditions. Methods The model of ischemia-reperfusion injury in skeletal muscle was created by clipping the right common iliac artery in rats. NSMA (3-nitro-N-methyl salicylate Amide) re-gastrocnemius muscle mitochondria RCR. Results Compared with the control group, the RCR decreased in groups 2, 3, 5 and 6 (P <0.01), and the difference was significant (P> 0.05). There was no significant difference in the RCR between the 4 groups and the control group RCR decreased (P <0.05), the difference was significant. Each drug than the corresponding group of mitochondrial RCR was significantly improved. Conclusion After ischemia-reperfusion, mitochondrial activity was significantly decreased and the degree of oxidative phosphorylation was decreased. The results suggest that NSMA may affect the electron transport in the respiratory chain and reduce the production of oxygen free radicals, thus improving mitochondrial activity during ischemia-reperfusion .