Effects of Hct on L-NAME-induced potentiation of anaphylactic presinusoidal constriction in perfused rat livers.

Effects of hematocrit (Hct) on N-nitro-L-arginine methyl ester (L-NAME)-induced modulation of anaphylactic venoconstriction were determined in isolated perfused rat livers. The rats were sensitized with ovalbumin (1 mg), and the livers were excised 2 weeks later and perfused portally and recirculatingly under constant flow at Hct of 0%, 5%, 16%, and 22%. The hepatic sinusoidal pressure was estimated via the double occlusion pressure (Pdo), and the presinusoidal resistance (Rpre) and the postsinusoidal resistance (Rhv) were calculated. The antigen of ovalbumin 0.1 mg was injected into the reservoir at 10 minutes after pretreatment with L-NAME (100 microM) or D-NAME (100 microM). Perfusate viscosity, a determinant of vascular resistance and shear stress, was increased in parallel with Hct. In the D-NAME groups, antigen caused predominant presinusoidal constriction. The magnitude of venoconstriction was significantly smaller at Hct 0% than at Hct 5% to 22%, whereas no significant differences were found among Hct 5% to 22%. L-NAME potentiated the antigen-induced increase in Rpre, but not in Rpost at Hct 5% to 22% as compared with D-NAME. But the augmentative effects of L-NAME were similar in magnitude among Hct 5% to 22%. These findings suggest that hepatic anaphylaxis increases production of nitric oxide, which consequently attenuates anaphylactic presinusoidal constriction in rat livers, and that these effects are independent of perfusate Hct or viscosity in blood-perfused rat livers.