Circulatory effects of graded diversion of portal blood flow to the systemic circulation in rats: role of nitric oxide.

Total portal-systemic shunting in normal animals is associated with splanchnic and systemic vasodilation, suggesting that vasodilation in cirrhosis may be facilitated by spontaneous shunts promoted by portal hypertension. However, the mechanism of this vasodilation is unknown. The aim is to study the acute effects of the graded diversion of portal blood flow to the systemic circulation in normal and portal hypertensive rats. Portal and systemic hemodynamics were measured in normal and portal hypertensive rats before and during graded portacaval diversion of portal blood flow, in basal conditions, and after nitric oxide inhibition. In portal hypertensive rats, graded portal flow diversion caused a rate-related decrease in portal pressure (from 15.3 +/- 0.6 to 11.2 +/- 0.7 mm hg at 6 mL x min(-1), P < .001) and a redistribution of portal-collateral blood flow from the spontaneous portal-systemic collaterals to the portacaval circuit, without changing total portal-systemic shunting. Graded portal diversion caused an immediate systemic vasodilation, with reduced peripheral resistance. This vasodilatory response was more pronounced in normal than in portal hypertensive rats (increase in cardiac index 23.6% +/- 2.8% vs. 8.5% +/- 4.9%, P < .02, fall in peripheral resistance -24.5% +/- 3.4% vs. -16.5% +/- 2.6%, P = .08), and was totally prevented by nitric oxide inhibition. The graded diversion of portal blood flow caused a flow-rate-related reduction in portal pressure and blood flow through spontaneous portal-systemic collaterals in portal hypertensive rats, and caused a nitric-oxide dependent systemic vasodilatory response, which was greater in normal than in portal hypertensive rats. These results suggest that portal-systemic shunting per se may contribute to the vasodilatation in portal hypertension.