PURPOSE: Hepatic dysfunction is associated with morbidity and mortality in critically ill patients. Understanding liver hemodynamics in pathological states requires characterization of the normal portal venous and hepatic arterial circulations. Using pressure flow analysis, we tested the hypothesis that vascular waterfalls determine blood flows in the normal liver. METHODS: In 14 vascularly isolated porcine livers, steady-state pressure-flow relationships, which defined a slope (incremental resistance) and a zero flow pressure intercept (Po), were generated for each vessel over a range of hepatic venous pressures (Phv). RESULTS: Critical closing pressures occurred in the portal venous circulation (Po = 3.8 +/- 0.4 mm Hg) with classical waterfall physiology observed as Phv was raised. The hepatic arterial critical closing pressure (Po = 8.3 +/- 1 mm Hg) showed a constant positive pressure difference of mm Hg versus Phv as the latter was increased from 0 to 28 mm Hg (P < .05). Portal venous resistance decreased when Phv was greater than Po (P < .05), but no effect on hepatic arterial resistance was seen as Phv was increased. CONCLUSION: Both critical closing pressures and incremental resistances showed markedly different responses to increased outflow pressures in the portal venous and hepatic arterial circulations. The results provide the physiological basis to analyze hemodynamic changes in the liver under normal and pathological conditions.
PURPOSE:Hepatic dysfunction is associated with morbidity and mortality in critically illpatients. Understanding liver hemodynamics in pathological states requires characterization of the normal portal venous and hepatic arterial circulations. Using pressure flow analysis, we tested the hypothesis that vascular waterfalls determine blood flows in the normal liver. METHODS: In 14 vascularly isolated porcine livers, steady-state pressure-flow relationships, which defined a slope (incremental resistance) and a zero flow pressure intercept (Po), were generated for each vessel over a range of hepatic venous pressures (Phv). RESULTS: Critical closing pressures occurred in the portal venous circulation (Po = 3.8 +/- 0.4 mm Hg) with classical waterfall physiology observed as Phv was raised. The hepatic arterial critical closing pressure (Po = 8.3 +/- 1 mm Hg) showed a constant positive pressure difference of mm Hg versus Phv as the latter was increased from 0 to 28 mm Hg (P < .05). Portal venous resistance decreased when Phv was greater than Po (P < .05), but no effect on hepatic arterial resistance was seen as Phv was increased. CONCLUSION: Both critical closing pressures and incremental resistances showed markedly different responses to increased outflow pressures in the portal venous and hepatic arterial circulations. The results provide the physiological basis to analyze hemodynamic changes in the liver under normal and pathological conditions.