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观察失血性休克大鼠重要生命器官细胞能量代谢的变化及超氧化物歧化酶(SOD)的保护作用。发现:随着休克的进展,大鼠心、肝、肾组织三磷酸腺苷(ATP)、磷酸激酶(CP)含量呈进行性减少,至休克2h,较对照组显著降低。经SOD治疗后,其含量明显增加,接近或达到正常水平,SOD并能显著提高休克动物的时间存活率及延长其存活时间。结果提示:氧衍生自由基的反应性损伤,可能是失血性休克细胞能量代谢障碍的重要原因;静脉注射SOD能有效地对抗氧自由基的这种损伤作用,从而保护休克时的能量代谢。
To observe the change of energy metabolism and the protective effect of superoxide dismutase (SOD) in the vital organs of hemorrhagic shock rats. It was found that with the progress of shock, the content of adenosine triphosphate (ATP) and phosphokinase (CP) in the heart, liver and kidney of rats decreased progressively to 2h after shock, which was significantly lower than that of the control group. After SOD treatment, its content increased significantly, approaching or reached the normal level, SOD and can significantly improve the time-survival rate of shock animals and prolong their survival time. The results suggest that the reactive oxygen species derived from reactive injury may be an important cause of energy metabolism disorder in hemorrhagic shock cells. Intravenous injection of SOD can effectively counteract this injury of oxygen free radicals and thus protect the energy metabolism during shock.