Reduction of intrahepatic vascular space in the pathogenesis of portal hypertension. In vitro and in vivo studies in the rat.

To elucidate a possible role for reduction of intrahepatic vascular space in the pathogenesis of portal hypertension, we studied a partially hepatectomized rat model in vitro and in vivo. The in vitro study used livers from normal, 1/3-hepatectomized, and 2/3-hepatectomized rats, and rats with cirrhosis caused by chronic bile duct ligation, for isolated, perfused flow-pressure plotting. Resistance to perfusion increased such that significant differences were found between all groups except the last two, which showed similar resistances. The in vivo study measured splanchnic blood flow by radioactive microspheres and portal pressure in anesthetized sham-operated and 1/3- and 2/3-hepatectomized rats. Although absolute portal tributary blood flows did not change, portal flow per gram of remnant liver showed significant increases: 1.57 +/- 0.32 ml/min X g liver, 2.52 +/- 0.60 ml/min X g liver, p less than 0.01; 3.48 +/- 1.04 ml/min X g liver, p less than 0.01, respectively. Although intrahepatic resistance increased significantly only in the 2/3-hepatectomized group, portal pressures increased significantly in both groups of hepatectomized rats: normal, 7.5 +/- 1.1 mmHg; 1/3-hepatectomized, 9.4 +/- 1.1 mmHg; and 2/3-hepatectomized, 11.1 +/- 1.2 mmHg. Thus, decreased intrahepatic vascular space caused by resection and hepatocellular hypertrophy leads to portal hypertension, thereby suggesting that this reduction in space may be the pathogenic factor common to a number of different theories of portal hypertension.