一氧化氮对缺血再灌注大鼠肾脏缺血预处理保护作用的贡献。

Toshihisa Ogawa, A. K. Nussler, Eda Tuzuner, Peter Neuhaus, Michio Kaminishi, Yoshikazu Mimura, Hans G. Beger
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引用次数: 59

摘要

我们研究了一氧化氮(NO)在缺血预处理(IP)对肾功能的影响以及缺血再灌注(I/R)介导的肾损伤中的血流动力学。缺血4分钟,再灌注间隔30分钟。I/R治疗包括30分钟缺血和60分钟再灌注间隔。我们测量了IP+I/R和I/R肾脏的肾小球滤过率(GFR)、钠的分数排泄(FE(Na))和肾血流量(RBF)。大鼠分别用NaCl、N(G)-硝基- l -精氨酸甲酯(L-NAME)或l -精氨酸预处理。我们发现,与I/R处理相比,IP显著改善了GFR和FE(Na);然而,L-NAME注射完全消除了这种作用,l -精氨酸处理增强了这种作用。L-NAME处理显著降低RBF,但没有改变亚硝酸盐/硝酸盐排泄。此外,我们发现单独使用IP不能诱导NO合成酶蛋白的表达,而使用I/R或IP+I/R处理可以明显诱导NO合成酶蛋白表达。此外,我们观察到与I/R处理相比,IP+I/R肾脏中血红素氧化酶-1的表达增加。我们的研究结果清楚地表明,IP预处理可以保护肾脏免受I/R介导的组织损伤,而这些作用部分是由NO介导的。
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Contribution of nitric oxide to the protective effects of ischemic preconditioning in ischemia-reperfused rat kidneys.
We examined the contribution of nitric oxide (NO) to the effect of ischemic preconditioning (IP) on renal function and the hemodynamics in ischemia-reperfusion (I/R) mediated kidney injury. IP was performed by using 4 minutes of ischemia followed by a 30-minute reperfusion interval. I/R treatment consisted of a 30-minute ischemia and 60-minute reperfusion interval. We measured the glomerular filtration rate (GFR), the fractional excretion of sodium (FE(Na)), and the renal blood flow (RBF) in IP+I/R and I/R kidneys. Rats were pretreated with NaCl, N(G)-nitro-L-arginine methyl ester (L-NAME), or L-arginine. We found that IP significantly improved GFR and FE(Na) as compared with I/R treatment; however, this effect was completely abolished by L-NAME injection and enhanced by L-arginine treatment. L-NAME treatment significantly diminished RBF but did not alter nitrite/nitrate excretion. Furthermore, we found that IP alone does not lead to inducible NO synthase protein expression whereas I/R or IP+I/R treatment clearly did. Moreover, we observed an increased heme oxygenase-1 expression in IP+I/R kidneys as compared with I/R treated ones. Our results clearly showed that IP pretreatment protects kidneys from I/R mediated tissue injury and that these effects were partially mediated by NO.
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