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Nitric oxide modulates renal vascular function in the marginal brain death donor
Author(s) -
Andrasi Terezia B,
Stumpf Nicole,
Reinerth Guenther,
Albers Joerg,
Vahl Christian F
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a336-a
Subject(s) - medicine , vasoconstriction , endocrinology , nitric oxide , vasodilation , endothelial dysfunction , kidney , renal function , transplantation , nitrite , chemistry , organic chemistry , nitrate
Vascular endothelial dysfunction occurs in the kidney graft coming from marginal brain death donors and may be responsible for a low success rate after transplantation. Brain death (BD) was induced in 16 dogs for 6 hours. Immediately after the inflation of the intracranial balloon, the treated group (n=6) received 40 mg/kg bolus followed by 3 mg/kg/min infusion of L‐arginine for 30 min. During BD progressive renal dysfunction was observed that coincided with a significant vasoconstriction, increase in renal venous nitrite (4.9 ±0.8 vs. 2.6±0.1, p<0.05) and MPO levels (1.43±0.04 vs. 2.43±0.23, p<0.001), and reduced vasodilatation of renal artery to Ach. Administration of L‐arginine counteracted the significant renal vasoconstriction induced by 6 hour BD (RVR=0.92±0.06 vs. 1.38±0.003 in controls, p<0.05), maintained renal ExtO 2 in physiological range (17.5±4.6% vs. 25.4±2.9% in controls, p<0.05), prevented the rise of MPO (1.69±0.19, p<0.05 vs. controls) and nitrite levels (3.3±0.5, p<0.05), and finally maintained endothelium dependent vasodilatation at pre‐BD values (p<0.05 vs. controls). Renal vascular dysfunction associated with altered NO metabolism occurs in brain death at a late stage due to increased oxidative stress. This derrangement seems to be in part prevented by exogenous L‐arginine supplementation.