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采用部分结扎腹主动脉的方法复制了低灌注型急性缺血性肾功能衰竭动物模型,并探讨了外源性还原型谷胱甘肽对其发病过程的影响。对照组大鼠肾在低灌注60 min(灌注压4 kPa)及再灌注1h 后的菊糖清除率为0.19±0.07 ml/min,显著低于治疗组(0.32+0.08 ml/min),再灌注24h 后,其血肌酐浓度及肾脏形态学半定量积分高于治疗组(分别为217±43μmol/L 和166±40μmol/L,4.4±0.9分和2.7±0.8分)。两组大鼠肾脏在再灌注15min 时其皮质丙二醛含量与其低灌注前水平相比无显著差异。结果提示,外源性还原型谷胱甘肽对低灌注后再灌注肾脏有保护作用,其机理可能并非是减轻自由基所致的损伤。
The animal model of hypoperfusion acute ischemic renal failure was reproduced by partial ligation of the abdominal aorta and the effect of exogenous reduced glutathione on its pathogenesis was explored. The inulin clearance rate of control rats was 0.19 ± 0.07 ml / min after 60 min of perfusion (perfusion pressure 4 kPa) and 1 h of reperfusion, which was significantly lower than that of the treatment group (0.32 ± 0.08 ml / min) After 24 hours, the serum creatinine concentration and the semi-quantitative morphological score of kidney were higher than those of the treatment group (217 ± 43μmol / L and 166 ± 40μmol / L, 4.4 ± 0.9 and 2.7 ± 0.8 respectively). There was no significant difference in the content of malondialdehyde in the cortex between the two groups at 15 min after reperfusion. The results suggest that exogenous reduced glutathione has a protective effect on reperfused kidneys after hypoperfusion, and its mechanism may not be to alleviate the damage caused by free radicals.