Exogenous nitric oxide protects kidney from ischemia/reperfusion

Blockade of NO production is followed by an increase in leukocyte rolling and adhesion resulting in some deleterious effects of ischemia. Preischemic administration of NO protects vascular integrity after reperfusion. Exogenous NO causes a direct reduction in leukocyte adhesion. This work was performed to test the hypothesis that exogenous NO administered during the preischemic period to the kidney alone, without coming into contact with the leukocytes, could also reduce leukocyte-endothelium adhesion. Adult rats were subjected to in situ isolation of the left kidney. Solutions were infused through the renal artery and drained through an incision in the renal vein, thus avoiding the systemic circulation. Group IC rats served as an ischemic control, and received 0.9% saline. Group NP received Na nitroprusside. Group S was a nonischemic control. Groups IC and NP were subjected to 75 min of renal ischemia. After this period, vascular structures were repaired and reperfusion allowed. A right nephrectomy was performed. Serum urea and creatinine, myeloperoxidase activity, and histopathological studies were carried out at different intervals after reperfusion. Survival at 15 days was 46%, 80%, and 100% in groups IC, NP, and S, respectively. Differences between groups for serum urea and creatinine were significant only during the first seven days. Myeloperoxidase values were significantly higher in group IC. All rats from group IC and only 20% from group NP showed histological evidence of necrosis. Thus, exogenous NO is protective and acts selectively upon the kidney, modulating its interactions with polymorphonuclear cells after ischemia/reperfusion.