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本文采用离体低灌再灌注肾技术探讨氧自由基在急性肾损伤中的致病作用以及钙拮抗剂间尼索地平（ｍ－Ｎｉｓ）的保护作用。低压（２．０～２．７ｋＰａ）灌注１小时后，继以１３．３ｋＰａ灌注１小时，肾皮质氧自由基清除剂超氧化物歧化酶（ＳＯＤ）活性明显降低，自由基代谢产物两二醛（ＭＤＡ）、Ｃａ含量及肾灌注阻力明显增加；低灌后再灌注时投以不同剂量的间尼索地平（０．０５μｍｏｌ／Ｌ与０．１μｍｏｌ／Ｌ）呈剂量依赖性地提高ＳＯＤ活性，降低ＭＤＡ、Ｃａ含量及肾灌注阻力。
In this study, the renal pathological changes of oxygen free radicals in acute kidney injury and the protective effect of m-Nis were explored by using the renal perfusion method. One hour after perfusion with low pressure (2.0 ~ 2.7kPa), the activity of superoxide dismutase (SOD) in renal cortical oxygen free radical scavenger decreased significantly after 1 hour of perfusion with 13.3 kPa. The free radical metabolite dialdehyde (MDA), Ca content and renal perfusion resistance significantly increased; low perfusion and reperfusion perfusion with different doses of nisoldipine (0.05μmol / L and 0.1μmol / L) in a dose-dependent manner to improve the activity of SOD, Reduce MDA, Ca content and renal perfusion resistance.