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RESEARCH PRODUCT

Progressive Development of Renal Vascular Dysfunction in Brain Death Implicates Reversible Alterations of Nitric Oxide Metabolism

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Vascular endothelial dysfunction occurs in the kidney graft from marginal brain death (BD) donors and may be responsible for a low success rate after transplantation.BD was induced in 16 dogs for 6 hours. Immediately after the inflation of the intracranial balloon, the treated group (n = 8) received 40 mg/kg bolus followed by 3 mg/kg/min infusion of L-arginine for 30 minutes. Renal vascular function and hemodynamic and biochemical parameters were determined.BD caused vasoconstriction, increase in renal venous nitrite (4.9 ± 0.8 versus 2.6 ± 0.1, P.05) and myeloperoxidase levels (1.43 ± 0.04 versus 2.43 ± 0.23, P.001), and reduced vasodilatation of renal artery to acetylcholine. Larginine diminished the renal vasoconstriction induced by 6 hour BD (RVR = 0.92 ± 0.06 versus 1.38 ± 0.003 in controls, P.05), maintained renal oxygen extraction in physiological range (17.5 ± 4.6% versus 25.4 ± 2.9% in controls, P.05) and prevented the rise of myeloperoxidase (1.69 ± 0.19, P.05 versus controls) and nitrite levels (3.3 ± 0.5, P.05), followed by preservation of endothelium dependent vasodilatation (P.05 versus controls).The findings suggest that exogenous L-arginine supplementation may preserve endothelial vascular function in the kidney before prelevation from marginal BD donors.