Present investigations support major contributions from increases in both portal blood flow and portal vascular resistance in the mechanism that maintains portal hypertension. B-Adrenergic blockers have been shown to reduce the elevated portal blood flow component. The possibility that nitroglycerin administration could reduce the elevated portal vascular resistance component is investigated here. Portal hypertension was induced in rats by a calibrated constriction of the portal vein. Portal hypertensive rats receiving placebo exhibited significant (p < 0.05) elevations over normal rats receiving placebo in cardiac index, portal venous inflow and portal pressure. Portal hypertensive rats were then divided into groups receiving nitroglycerin infusion, propranolol (Badrenergic blockade) and combined administration of nitroglycerin and propranolol. Significant reductions (p < 0.05) in portal blood flow of 30, 32 and 44%, respectively, were accompanied by significant portal pressure reductions of 2.7 f 0.2, 1.7 f 0.3 and 3.6 f 0.4 mm Hg in all groups, respectively (p < 0.05). Nitroglycerin failed to prevent a 46% rise in portal-collateral resistance accompanying the portal blood flow reduction, similar to resistance rises also found in propranololtreated (33%) and combination nitroglycerin-propranolol-treated (49%) groups. We conclude that nitroglycerin infusion can significantly reduce portal pressure, alone or in combination with 8blockade, by reducing portal venous inflow. It appears that nitroglycerin reduces portal blood flow through the effect of baroreceptor sympathetic reflexes that constrict the splanchnic bed in response to vasodilatation and venous pooling.
Portal pressure is the result of the interplay between portal blood flow and the vascular resistance offered to that flow. Present investigations from this laboratory and other laboratories (1-5) support major contributions from increases in both portal blood flow and vascular resistance in the mechanisms that maintain portal hypertension. While it is possible to reduce portal pressure by reducing portal blood flow using /3-blockers, complete correction of portal hypertension cannot be achieved by this sole approach. A rise in the vascular resistance of the portal-collateral system, during 8-blockade treatment, maintains portal pressure at abnormally high levels in spite of normalization of portal blood flow (6). In order to potentiate the portal pressure-reducing effect