The effects of nitric oxide on shock caused by temporary hepatic inflow occlusion in pigs

BACKGROUND/AIMS: Nitric oxide (NO) plays an important role in the regulation of systemic hemodynamics in various shock status. The effect of NO on shock induced by hepatic inflow occlusion has not been previously investigated. METHODOLOGY: We examined the effects of NO on systemic hemodynamics and oxygen metabolism in shock caused by temporary hepatic inflow occlusion without bypass in pigs using NO synthase inhibitor, NG-nitro-L-arginine methyl ester (NAME group) and the substrate for NO synthesis, L-arginine (ARG group). RESULTS: All animals in the control and ARG group tolerated the surgery, while 2 of 5 animals in the NAME group died during the occlusion period. Cardiac output and mixed venous oxygen saturation (SvO2) in the NAME group was significantly reduced compared with the other two groups during and after hepatic inflow occlusion. In contrast, SvO2 in the ARG group was maintained at higher levels throughout the study period, and the recovery time of cardiac output following reperfusion was earlier than that of the other two groups. CONCLUSIONS: Endogenous NO inhibition exacerbates the shock status induced by hepatic inflow occlusion. Exogenous administration of NO donor may improve the shock status induced by hepatic inflow occlusion.