Effects of nitric oxide on hemodynamic changes and metabolism following acute hepatic inflow occlusion in pigs

The purpose of this study was to examine the effects of nitric oxide on systemic hemodynamics and oxygen metabolism following acute hepatic inflow occlusion. Fourteen mongrel pigs received solvent (control group, n = 4), the nitric synthesis inhibitor N^G-nitro-L-arginine methyl ester (L-NAME group, n = 5), or the substrate for nitric oxide synthesis L-arginine (L-arginine group, n = 5) 30 min before hepatic inflow occlusion. Following 30 min of hepatic ischemia, all livers were reperfused. While all pigs in the control group and L-arginine group survived more than 7 days after reperfusion, two of five pigs in the L-NAME group died during hepatic ischemia period. However, venous oxygen saturation was significantly lower during and after ischemic period, oxygen extraction ratio was significantly higher during hepatic ischemic period in L-NAME group, and systemic vascular resistance was also significantly higher 5 and 15 min after hepatic inflow occlusion. Furthermore, lactate/pyruvate ratio was significantly higher during hepatic ischemic period in L-NAME group. In summary, inhibition of nitric oxide synthesis resulted in maintaining higher arterial blood pressure, but aggravated tissue oxygenation during and after hepatic inflow occlusion. We conclude that nitric oxide appears to decrease arterial blood pressure, but improve the tissue oxygenation in acute hepatic inflow occlusion and reperfusion.