Abstract
The effect of shear stress on nitric oxide (NO)-mediated attenuation of anaphylactic vasoconstriction was studied using an isolated guinea pig liver perfused under constant flow or pressure. The flow constant resulted in increased shear stress during constriction; the perfusion pressure steady prevented changes in shear stress. Using the double occlusion technique to estimate the hepatic sinusoidal pressure (Pdo), pre- (Rpre) and post-sinusoidal (Rpost) resistances were calculated. In either constant flow or pressure perfusion, anaphylaxis contracted predominantly pre-sinusoids over post-sinusoids, a finding consistent with the previous study (Ruan et al. Am J Physiol Regul Integr Comp Physiol, in press). When shear stress was allowed to rise, the presinusoidal constriction, but not post-sinusoidal constriction, was significantly potentiated after NO synthase blockade using NG-nitro-L-arginine methyl ester (L-NAME, 100 μM). When shear stress was held constant by maintaining constant perfusion pressure, L-NAME potentiated both pre- and post-sinusoidal constriction in a similar magnitude. The data suggest that hepatic anaphylaxis generates NO in a shear stress independent manner, resulting in dilatation of both pre- and post-sinusoidal vessels. In contrast, NO was preferentially generated shear stress dependently at the vigorously contracted pre-sinusoids and dilate predominantly that pre-sinusoids in isolated guinea pig liver with anaphylactic venoconstriction. [Jpn J Physiol 54 Suppl:S92 (2004)]
