摘要
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。
Alteration in energy metabolism of the vital or- gans and the protective effect of superoxide dismutase (SOD) were observed in rats with hemorrhagic shock. With the development of shock, gradual de- crease in energy levels was found in the heart, liver, and kidney. The contents of ATP and CP in these or- gans of the rats which had been in shock for two hours were significantly low as compared with those in the control group. After giving SOD intravenously, the rats were found to have a remarkable increase in tissue energy level and time survival rate. The results suggest that the oxygen-derived free radicals may play an im- portant role in impaired cellular energy metabolism in hemorrhagic shock, and that intravenous injection of SOD can effectively protect mltochondria from this ef- fect of the free radicals and improve energy metabolism in hemorrhagic shock.
出处
《中国危重病急救医学》
CAS
CSCD
1993年第5期269-271,共3页
Chinese Critical Care Medicine
基金
国家自然科学基金
关键词
超氧物歧化酶
休克
出血性
代谢
superoxide dismutase
energy metabolism
hemorrhagic shock