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 sp lanchnic and systemic vasodilation, suggesting that vasodilation in ci rrhosis may be facilitated by spontaneous shunts promoted by portal hy pertension. However, the mechanism of this vasodilation is unlinown. T he aim is to study the acute effects of the graded diversion of portal blood flow to the systemic circulation in normal and portal hypertens ive rats. Portal and systemic hemodynamics were measured in normal and portal hypertensive rats before and during graded portacaval diversio n of portal blood flow, in basal conditions, and after nitric oxide in hibition, In portal hypertensive rats, graded portal flow diversion ca used a rate-related decrease in portal pressure (from 15.3 +/- 0.6 to 11.2 +/- 0.7 mm hg at 6 mL.min(-1), P < .001) and a redistribution of portal-collateral blood flow from the spontaneous portal-systemic coll aterals to the portacaval circuit, without changing total portal-syste mic shunting. Graded portal diversion caused an immediate systemic vas odilation, with reduced peripheral resistance. This vasodilatory respo nse was more pronounced in normal than in portal hypertensive rats (in crease in cardiac index 23.6% +/- 2.8% vs. 5.5% +/- 4.9%, P < .02, fal l in peripheral resistance -24.5% +/- 3.4% vs, -16.5% +/- 2.6%, P = .0 8), and was totally prevented by nitric oxide inhibition, The graded d iversion of portal blood flow caused a flow-rate-related reduction in portal pressure: and blood flow through spontaneous portal-system coll aterals in portal hypertensive rats, and caused a nitric-oxide depende nt systemic vasodilatory response, which was greater in normal than in portal hypertensive rats. These results suggest that portalsystemic s hunting per se may contribute to the vasodilatation in portal hyperten sion.