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目的 :检测一氧化氮合酶 (NOS :eNOS ,iNOS ,nNOS)在肾脏缺血预处理动物模型肾组织中的表达 ,探讨NOS在肾脏缺血预处理中的可能作用机制。方法 :将 36只小白兔随机分为四组即对照组、缺血预处理组(IP)、缺血再灌注组 (I/R)和缺血预处理后再灌注组 (IP +I/R)。分别检测各组肾组织中NOS的表达及组织学变化。结果 :在急性肾缺血 6 0min再灌注 6 0min时 ,eNOS阳性表达在IP组和IP +I/R组明显高于I/R组和对照组 (P <0 .0 1) ,iNOS和nNOS在组织肾中未见明显表达。组织学变化发现I/R组肾组织中肾细胞发生明显变性坏死 ,而IP组和对照组未见明显改变。结论 :肾脏缺血预处理在肾脏缺血再灌注中具有保护作用 ,而NOS参与该作用机制。
Objective: To investigate the expression of nitric oxide synthase (nNOS, iNOS, nNOS) in renal tissue of renal ischemic preconditioning animal model and to explore the possible mechanism of NOS in renal ischemic preconditioning. Methods: Thirty - six rabbits were randomly divided into four groups: control group, IP group, I / R group and IP + I / R). The expression of NOS and histological changes in each group were detected. Results: The expression of eNOS in IP group and IP + I / R group was significantly higher than that in I / R group and control group (P <0.01) at 60 min of reperfusion after 6 min of acute renal ischemia, and iNOS and nNOS No obvious expression in the tissue of kidney. Histological changes found in renal I / R group of renal cells were significantly degeneration and necrosis, while the IP group and the control group no significant change. Conclusion: Renal ischemic preconditioning has a protective effect on renal ischemia-reperfusion, and NOS participates in this mechanism.