Short communicationInhibition of nitric oxide synthesis enhances d-galactosamine-induced acute liver injury

Nitric oxide (NO), a potent vasodilator, also mediates a variety of physiological processes. We investigated the role of endogenous NO on d-galactosamine (d-Galn)-induced liver injury. Sixteen rats were divided into four treatment groups; (a) d-Galn plus Nω-nitro-l-arginine (l-NNA), (b) d-Galn plus Nω-nitro-d-arginine (d-NNA alone, and (d) d-NNA alone. d-Galn was administrated intraperitoneally at a dose of 1000 mg/kg at time 0, and arginine derivatives were administrated intraperitoneally at a dose of 40 mg/kg at the same time and at 8 h intervals. After 48 h, regional hepatic blood flow and serum levels of aspartate aminotransferase and alanine aminotransferase were measured. Serum levels of AST and ALT in rats treated with d-Galn plus l-NNA were significantly higher than those in rats treated with d-Galn plus d-NNA. Regional hepatic blood flow in rats treated with d-Galn plus l-NNA was significantly decreased compared with those in rats treated with d-Galn plus d-NNA. Treatment with d-NNA and l-NNA alone had no adverse effects on serum AST and ALT levels and regional hepatic blood flow. These results suggest that endogenous NO has a protective effect on d-Galn-induced liver injury through a maintenance of hepatic microcirculation.