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目的：了解NO在缺血预处理（IPC）抗缺血再灌注（IR）肾损伤中的作用，进一步探讨IPC对IR肾损伤的保护机制。方法：将23只日本大耳白兔分为对照、缺血再灌流（IR）和缺血预处理（IPC）＋IR三组，分别观察其血浆和肾组织中一氧化氮（NO）、肌酐（CRE）和尿素氮（BUN）等含量的变化。结果：IPC＋IR组的NO含量高于IR组（P＜0．05），CRE和BUN含量低于IR组（P＜0．05）；三项指标在IPC＋IR组同对照组间差异均无显著性（P＞0．05）。肾组织超微结构的损害IPC＋IR组轻于IR组。结论：结果提示IPC可使IR肾损伤程度减轻，其机制可能同NO的扩血管和清除氧自由基等作用有关。
OBJECTIVE: To investigate the role of nitric oxide in ischemic preconditioning (IPC) against renal ischemia-reperfusion injury (IR) and to explore the protective mechanism of IPC on IR renal injury. Methods: Twenty-three Japanese white rabbits were divided into three groups: control, ischemia reperfusion (IR) and ischemic preconditioning (IPC) + IR. Nitric oxide (NO) and creatinine CRE) and urea nitrogen (BUN) content changes. Results: The content of NO in IPC + IR group was higher than that in IR group (P <0.05), and the contents of CRE and BUN were lower than those in IR group (P <0.05). There was no significant difference in the three indexes between IPC + IR group and control group (P> 0.05). The damage of renal ultrastructure IPC + IR group lighter than IR group. Conclusions: The results suggest that IPC can reduce IR renal injury, the mechanism may be related to NO vasodilatation and scavenging oxygen free radicals.