Protective effect of exogenous nitric oxide on the renal function and inflammatory response in a model of ischemia-reperfusion.

摘要: Background. Tissue subjected to a period of ischemia undergoes morphological and functional damage that increases during the reperfusion phase. The aim present work was assess possible improvement induced by exogenous administration nitric oxide (NO) on renal injury inflammatory reaction in an experimental animal model ischemia-reperfusion (I-R). Methods. Ischemia achieved ligation left arteria vein for 60 min, followed first contralateral nephrectomy then reestablishment blood flow. Molsidomine, used as NO donor, administered systemic injection 30 min before reperfusion. effect molsidomine compared with hydralazine, non-NO donor hypotensive agent. Results. Treatment improved dysfunction (increase plasma creatinine urea levels) caused I-R. Moreover, blunted enhanced production proinflammatory cytokines (tumor necrosis factor [TNF]-α interleukin [IL] 1α), increase tissular levels superoxide anions oxygen free radical scavengers, neutrophilic infiltration observed ischemic kidney. One hundred percent survival group animals treated whereas groups undergoing I-R did not receive showed 40% mortality from second day after Conclusions. demonstrated treatment function diminished responses kidney process.