We tried to establish an animal model of portal venous thrombosis in order to analyze the ensuing pathological changes of the liver. An emulsion with Escherichia coli endotoxin and Lipiodol-Ultra-Fluide was injected into the portal vein of the left anterior lobe of the rabbit liver. The target lobe and portal vein were time-sequentially examined. In the experimental groups, it was found that fibrin thrombi were formed in the portal vein within 48 h after the injection and thrombi persisted for over 7 days. In an association with thrombus formation, numerous tortuously dilated vasculatures developed in the portal tract (cavernomatous vasculature) within 48 h. Both the number and the total area of the cavernomatous vasculatures increased from 2- to 3-fold more than in the control group at 72 h. The majority of proliferated vasculatures were positive for alpha-smooth muscle actin, thus suggesting that they derived from the portal venous branches. In conclusion, portal endotoxemia may be one of the pathogenetic factors of portal venous thrombosis and, in this model, the cavernomatous vasculatures rapidly developed from the portal venous branches.