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目的：探讨急性缺血再灌流（IR）肾损伤的机理。方法：18只日本大耳白兔随机分为对照组、IR组。采用左肾切除，右肾动静脉夹闭1h再灌流3h致肾损伤模型。结果：IR组血和肾组织中丙二醛（MDA）及肾组织中WBC滞留数、肾小管计分和Na＋、Ca2＋浓度较对照组显著升高（P＜0．05）。血和肾组织SOD活力，肾组织NO含量显著降低（P＜0．05）。IR组有明显的组织学损伤改变。结论：氧自由基生成增多、NO减少和WBC滞留导致的无复流现象及Na＋、Ca2＋超载等因素参与了IR肾损伤。
Objective: To investigate the mechanism of acute kidney injury after ischemia-reperfusion (IR). Methods: Eighteen Japanese white rabbits were randomly divided into control group and IR group. Left kidney resection, right renal artery and vein occlusion 1h reperfusion 3h induced renal injury model. Results: The levels of malondialdehyde (MDA), renal tubular WBC retention, renal tubular score and Na +, Ca2 + in IR group were significantly higher than those in control group (P <0.05). SOD activity in blood and kidney tissue and NO content in renal tissue were significantly decreased (P <0.05). IR group had obvious histological changes. CONCLUSIONS: There is an increase in oxygen free radicals, NO reduction and WBC retention-induced no-reflow phenomena and Na +, Ca2 + overload and other factors involved in IR kidney injury.