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缺血肾组织再灌后原缺血损害加重，其机理不详，亦无良好方法预防。本实验通过测定肾组织丙二醛（ＭＤＡ）、超氧化物歧化酶（ＳＯＤ）活性，发现缺血肾再灌后ＭＤＡ较正常肾或单纯缺血肾明显升高，ＳＯＤ的活性显著下降；ＶｉｔＥ或辅酶Ｑ１０能抑制再灌后ＭＤＡ的升高，并改善肾组织超微结构的损伤。结果表明：肾缺血再灌时产生的大量氧自由基导致了肾再灌性损害。
Ischemia reperfusion of ischemic renal tissue increased severity of its mechanism is unknown, there is no good way to prevent. In this experiment, the activity of malondialdehyde (MDA) and superoxide dismutase (SOD) in renal tissue was measured. MDA was found to be significantly higher than normal kidney or pure ischemic kidney after ischemia reperfusion, and the activity of SOD was significantly decreased. VitE Or coenzyme Q10 can inhibit MDA increased after reperfusion, and improve renal tissue ultrastructure damage. The results show that a large number of oxygen free radicals generated during renal ischemia-reperfusion lead to renal reperfusion injury.