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目的：探讨肾缺血再灌流损伤发生的机制。方法：采用家兔急性肾缺血再灌流损伤模型，实验分缺血再灌流（IR）组和对照（control）组。均去右肾，检测在缺血1小时后再灌流24小时时肾组织中过氧化脂质（LPO）、血清中肌研（Cr）和尿素氮（BUN）含量；光镜下肾组织中白细胞（WBC）和肾小管坏死数目；电镜下肾组织超微结构改变。结果：IR组以上指标同对照组比较，差异显著（P＜0.01）；IR组肾组织细胞发生明显变性、坏死改变，而对照组肾组织超微结构正常。结论：肾组织中WBC和氧自由基增多在缺血再灌流性肾损伤中起着重要的作用。
Objective: To investigate the mechanism of renal ischemia-reperfusion injury. Methods: The model of acute renal ischemia / reperfusion injury in rabbits was divided into experimental group (ischemia / reperfusion group and control group). The contents of lipid peroxidation (LPO), serum creatinine (Cr) and blood urea nitrogen (BUN) in kidneys were measured at 1 hour after ischemia and 24 hours after reperfusion. WBC) and the number of renal tubular necrosis; ultrastructure changes of renal tissue under electron microscope. Results: Compared with the control group, the above indexes of IR group were significantly different (P <0.01). Renal cells were significantly degeneration and necrosis in IR group, while the ultrastructure of kidney in control group was normal. Conclusion: Increased WBC and oxygen free radicals play an important role in renal ischemia-reperfusion injury.