Objective To evaluate the feasibility of establishing portal vein thrombosis model in cirrhotic rats. Methods SD rats were randomly divided into model group and blank group. Cirrhosis model was first established in the model group. On this basis, portal vein thrombosis model was established by intermittent portal vein ligation combined with clamp. The portal vein thrombosis was confirmed by hepatic color Doppler ultrasonography 1 week after modeling. Then the model group was randomly divided into model control group and model recovery group. Liver and portal vein were extracted from model control group and blank control group after laparotomy, and liver and portal vein were extracted from model recovery group after continued feeding for 2 weeks. Liver and portal vein samples in each group were stained with HE, Masson and portal vein elastic fiber (EVG). Results Ultrasound examination showed that stable thrombus formed in the portal vein of the model group one week after operation, and the success rate of modeling was 68%. HE and Masson staining showed false lobules and portal vein thrombosis, media edema and thickening, collagen fiber adhesion, EVG staining showed portal vein intimal injury in both model group and model recovery group. In the blank group, there was no thrombosis in the portal vein, and the vascular structure was intact. Through transmission electron microscopy, collagen fiber bundles were found in the hepatic sinuses of cirrhotic rats, and hepatocyte mitochondria were heterogeneous in size, with focal aggregation. Portal vein endotheliμm exfoliation, apoptosis, phenotypic migration of smooth muscle cells to the protoendotheliμm, subintimal fibrous tissue proliferation. At 3 weeks after operation, none of the rats in the model recovery group died and PVT remained stable. Conclusion The shedding of portal vein endotheliμm, intimal fibrosis, phenotypic smooth muscle cells and migration to intima are the important pathologic basis of portal vein thrombosis in cirrhosis. Using the intermittent ligation combined with clamp method, a stable rat model of portal vein thrombosis in liver cirrhosis can be successfully established on the basis of liver cirrhosis. The pathological changes, including vascular endothelial injury, intima thickening and fibrosis, and slow blood flow rate, are consistent with the formation mechanism of PVT in liver cirrhosis. And the model rats can survive for at least 3 weeks, providing a modeling method and survival time basis for deepening the study of portal vein thrombosis in liver cirrhosis.