抄録
Effects of a NO synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), on anaphylaxis-induced venoconstriction were examined in isolated rat liver perfused with blood of various hematocrit (Hct) to clarify the role of nitric oxide (NO) in anaphylactic venoconstriction in rat livers.The rats were sensitized with ovalbumin (1 mg), and two weeks later, the liver was excised and perfused portally and recirculatingly at a constant flow with blood at Hct of 0, 5, 16, and 22%. We measured the viscosity of perfusing blood. Using the double occlusion technique to estimate the hepatic sinusoidal pressure (Pdo), presinusoidal resistance (Rpre) and postsinusoidal resistance (Rhv) were calculated. The antigen, ovalbumin (0.1 mg), was injected into the reservoir 10 min after pretreatment with L-NAME (100 μM) or D-NAME (100 μM). The viscosity, a determinant of vascular resistance and shear-stress, increased in a Hct-dependent manner. L-NAME pretreatment increased exclusively basal Rpre in liver perfused at Hct 22%. The antigen caused hepatic venoconstriction as characterized by predominant presinusoidal constriction in all antigen administered livers. L-NAME pretreatment potentiated the antigen-induced venoconstriction, as compared with the D-NAME pretreatment, by increasing Rpre, but not Rpost. These finding suggests that hepatic anaphylaxis increased production of NO, which consequently attenuated anaphylactic presinusoidal venoconstriction in isolated perfused rat livers. [J Physiol Sci. 2006;56 Suppl:S135]
