ANATOMICAL LESIONS BEING RESPONSIBLE FOR DEVELOPMENT OF PORTAL HYPERTENSION IN CARBON TETRACHLORIDE-INDUCED RAT LIVER CIRRHOSIS

The hemodynamics of carbon tetrachloride-Induced rat liver cirrhosis were examined by means of the perfusion experiment and the anatomical lesions being responsible for the development of portal hypertension were evaluated. The portal blood flow of isolated rat liver was 3.07±0.53 ml/g/min. in intact rats, 1.94±0.24ml/g/min. In fibrosis rats and 1.75±0.23 ml/g/min. in cirrhosis rats under the condition of perfusion pressure 13.5 cmH₂O and of Ht 36%. The flbrotlc liver as well as cirrhotic liver showed marked elevation of hepatic vascular resistance, and more than 20 cmH₂O perfusion pressures were necessary for the fibrotlc liver as well as the cirrhotic liver to hold the normal level of hepatic blood flow. There was no perceptible stenosis or distortion of the Intrahepatic portal tree and of the hepatic venous tree, but there was marked constriction of the sinusoid resulting from enlargement of the hepatic cell in the fibrotlc liver as well as in the cirrhotic liver. The Intimate correlation between the hepatic blood flow reduction and the extent of sinusoidal constriction suggested that vascular resistance of cirrhotic liver was located In the sinusoidal bed.