一氧化氮在胰岛素抗急性缺血再灌注肾损伤中的作用研究

目的：观察NO在胰岛素抗急性缺血再灌注（IR）肾损伤中的作用，进一步探讨胰岛素减轻肾缺血再灌注损伤的作用及其机制。方法：采用肾动脉钳夹法建造急性缺血再灌注性肾损伤模型。将家兔分为对照组、单纯缺血再灌注（IR）组、胰岛素处理（Ins-IR)组。观测三组动物缺血再灌注2小时、48小时时，肾组织一氧化氮（NO）含量、血清尿素氮（BUN）水平、血清及肾组织中丙二醛（MDA）含量，和肾组织超微结构的改变。结果：肾缺血再灌注2小时和48小时时，IR组肾组织中NO含量明显降低（P＜0.001)，胰岛素处理组NO水平维持在正常水平。相应的缺血再灌注48小时时的血清尿素氮水平，IR组较对照组显著升高（P＜0.001)，Ins-IR组与对照组差异无显著性（P＞0.05)；血清及肾组织中MDA含量组较对照组显著升高（P＜0.05)，胰岛素处理组MDA含量明显降低（P＜0.05)；肾组织切片电镜观察显示，对照组超微结构无改变，IR组肾组织有变性和坏死，而Ins-IR组肾组织仅轻度变性。结论：促进NO的生成是胰岛素抗肾IR损伤的重要环节，可能与NO清除氧自由基，减轻肾组织IR损伤中的无复流现象等作用有关。

THE ROLE OF NITRIC OXIDE IN INSULIN ANTAGONIZING THE ACUTE RENAL INJURY OF ISCHEMIC-REPERFUSION

Objective: To observe the role of nitric oxide (NO) in insulin antagoning the acute renal injury induced by ischemic-reperfusion. Metholds: 27 Japanese white rabbits were allocated randomly into control group, ischemic-reperfusion group(IR group) and insulin treatment group(Ins-IR group). IR reperfusion. Insulin injection (3U/kg, glucose1.5g/kg, K + 4mg/kg) was administered intravenously to the Ins-IR group twice a day for two days, while only glucose saline in equal amount was administered to IR group and control group. At 2h or 48h after reperfusion, sugar and urea nitrogen(BUN) in serum, MDA in serum and renal tissue, nitric oxide (NO) in renal tissue were determined; the ultra-structure of renal tissue was observed under electron-microscope. Results: Plasma BUN of IR group was significantly higher than ahat of the control group after 48 hours of reperfusion(P<0.001); MDA contents in IR group were much higher than that in the control group (P<0.05), the concentration of NO in renal tissue was much lower than that the control group since the time of 2 hours reperfusion (P<0.001). Treatment with insulin considerably reduced the BUN, MDA level (P<0.05, compared with IR group); and greatly increased the NO level (P<0.05, compared with IR group). Under electron-microscope, the serious degeneration and necrosis of renal tissue were observed in IR group, but only slight degeneration in Ins-IR group. Conclusions: The results indicate that the increase of NO by insulin plays an important role in the protecting effect of insulin on renal ischemic-reperfusion injury