Blood viscosity and hepatic vascular resistance

Abstract

In order to clarify the relationship between blood viscosity and hepatic vascular resistance, the isolated normal and CCl4-induced rat livers were perfused with Krebs-Ringer bicarbonate buffer solution suspended with bovine erythrocytes (hematocrit of 0% to 65%). Portal vein pressures in vivo of the normal rat (128.0±2.4mmH₂O) and of the cirrhotic rat (180.5 ±10.1mmH₂O) approximated to the lowest perfusion pressures providing the minimum hepatic vascular resistance at hematocrit of 40% (economical perfusion pressure). In the cirrhotic liver the economical perfusion pressure elevated markedly with increasing hematocrit, especially over hematocrit of 40%, than in the normal liver. This is because that in the cirrhotic liver an increase in number of the narrow sinusoids less than 10μm in diameter led to elevation of the hepatic vascular resistance and the high viscosity of the perfusate. These experimental findings suggest that an increase in hematocrit may cause a prominent elevation of portal vein pressure in the patient with cirrhosis.