We determined whether the triple vascular occlusion pressure (Pto), the equilibration pressure obtained when the hepatic artery, portal, and hepatic veins were occluded simultaneously, represented the capillary pressure (Pc) in isolated bivascularly blood-perfused canine livers. Effects of a bolus injection of histamine (0.1-60 micrograms), norepinephrine (NE; 1-600 micrograms), or acetylcholine (ACh; 0.01-10 micrograms) into the portal vein or the hepatic artery were also studied on vascular resistance distribution using Pto as a measure of Pc. The livers were perfused at constant flow via the portal vein and at constant pressure via the hepatic artery. Pto was compared with Pc measured using the traditional gravimetric method (Pc,i). Pto and Pc,i showed a strong correlation (Pto = -0.02 + 0.98 Pc,i; r = 0.83, P = 0.0018). With comparisons, the intercept was not significantly different from zero, and the slope was not different from 1.00, indicating that Pto accurately represented Pc. The resting postsinusoidal vascular resistance comprised 54% of the total hepatic vascular resistance (Rt). Portal or arterial injection of histamine increased predominantly hepatic venous resistance (Rhv) over portal resistance with liver weight gain. NE constricted both the portal vein and the hepatic artery in greater magnitude than the hepatic vein, as evidenced by a significant decrease in the Rhv/Rt ratio. This precapillary constriction was accompanied by a significant decrease in liver weight. In contrast, ACh contracted both portal and hepatic veins similarly without liver weight change. We conclude that Pto is an excellent estimate of Pc in isolated blood-perfused canine livers and that the hepatic vascular resistance sites in the resting states are located evenly in the pre- and postsinusoidal vessels. Intraportal or intra-arterial infusion of histamine, NE, and ACh produced characteristically different changes in hepatic vascular resistances and hepatic volume. The Pto technique could be applied in experimental research on hepatic hemodynamics.

This study was designed to determine the effects of thromboxane A2 (TxA2) on the distribution of vascular resistance, lung weight, and microvascular permeability in isolated dog lungs perfused at a constant pressure with autologous blood. The stable TxA2 analogue (STA2; 30 micrograms, n = 5) caused an increase in pulmonary capillary pressure (Pc) assessed as double-occlusion pressure to 14.0 +/- 0.4 mmHg from the baseline of 7.9 +/- 0.3 mmHg with progressive lung weight gain. Pulmonary vascular resistance increased threefold exclusively due to pulmonary venoconstriction. Pulmonary venoconstriction was confirmed in lungs perfused in a reverse direction from the pulmonary vein to the artery (n = 5), as evidenced by marked precapillary vasoconstriction and a sustained lung weight loss. Furthermore, in lungs perfused at a constant blood flow (n = 5), STA2 also caused selective pulmonary venoconstriction. Vascular permeability measured by the capillary filtration coefficient and the isogravimetric Pc at 30 and 60 min after STA2 infusion did not change significantly from baseline in any lungs studied. Moreover, elevation of Pc by raising the venous reservoir of the intact lobes (n = 5) to the same level as the STA2 lungs caused a greater or similar weight gain compared with the STA2 lungs. Thus, we conclude that TxA2 constricts selectively the pulmonary vein resulting in an increase in Pc and lung weight gain without significant changes in vascular permeability in isolated blood-perfused dog lungs.