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本文测定了大鼠肾脏自身抗氧化能力在缺血再灌注过程中的变化。结果发现１ｈ的肾缺血（夹闭肾蒂）会造成肾皮质谷胱甘肽总含量及维生素Ｅ含量的下降。但肾皮质ＳＯＤ及ＧＳＨｐｘ活力未受显著性影响。继１ｈ后的１５ｍｉｎ再灌注显著地降低了ＳＯＤ及ＧＳＨｐｘ活力、皮质及血浆维生素Ｅ含量、皮质ＧＳＨ含量，而ＧＳＳＧ含量则显著升高。经尾静脉分别给大鼠ＤＦＯ及Ｃａｔ可显著改善大鼠肾脏的病理变化以及１ｈ缺血、２４ｈ再灌注后的血肌酐升高，并显著地保护了肾皮质ＳＯＤ及ＧＳＨｐｘ活力。结果提示缺血会造成肾脏自身抗氧化能力的降低，使用活性氧清除剂可缓解再灌注造成的肾脏组织及功能损伤。
This article measured the changes of renal antioxidant capacity in rats during ischemia-reperfusion. The results showed that 1h of renal ischemia (clipping of the renal pedicle) will cause renal cortical glutathione content and vitamin E levels decreased. However, renal cortex SOD and GSHpx activity was not significantly affected. Reperfusion at 15 min after 1 h significantly reduced SOD and GSHpx activity, cortical and plasma vitamin E levels, cortical GSH content, while GSSG content increased significantly. Rat DFO and Cat were respectively administrated into rat tail vein to improve the pathological changes of rat kidney, as well as the increase of serum creatinine after ischemia for 1 hour and reperfusion 24h, and significantly protected the activities of SOD and GSHpx in renal cortex. The results suggest that ischemia can cause the kidney to reduce its own antioxidant capacity, the use of reactive oxygen scavengers can alleviate renal tissue damage and reperfusion injury.