Distensibility of hepatic venous resistance sites and consequences on portal pressure.

Hepatic venous resistance was measured in cats anesthetized with pentobarbital sodium during changes in hepatic blood flow and in inferior vena cava (IVC) pressure, in an attempt to explain the variable and partial transmission of pressure from IVC to portal vein. Problems with earlier explanations based on a "vascular waterfall" or a "Starling resistor" are discussed. Our data and previously published data can be explained by the hypothesis that hepatic venous resistance decreases as the resistance site is distended by the pressure within the resistance vessels. The product of resistance and distending pressure was a constant. This constant equals the resistance at unit-distending pressure, and it is an index of active contraction of the resistance sites in acute experiments. It is increased during infusions of norepinephrine, and it is higher in innervated than in denervated livers. A distensible hepatic venous resistance is a passive mechanism for partial autoregulation of portal pressure. It also serves as a mechanism for regulation of the splanchnic capacitance response to changes in IVC pressure.