Objective To explore the effect of vascular endothelial growth factor (VEGF) on portal pressure in rats with Budd-Chiari syndrome (B-CS). Methods Male Sprague-Dawley (S-D) rats were used to make 30% narrow of the inferior vena cava by surgery. The experiments were divided into B-CS + VEGF group (group B, n=12), B-CS + normal saline group (group C, n=12) and sham operation group (group A, n=15). The animals in group B received continuous intravenous injection of VEGF (6 μg/kg body weight every day), and those in group A and C were given the same amount of normal saline for 4 weeks. The portal vein pressure was measured at 8th week postoperatively. Pathological changes of the liver were observed by HE staining. Intrahepatic vascular density was quantified by immunohistochemical staining. Results The rate of B-CS formation in rats was about 60%. B-CS rats showed obstruction of inferior vena cava and main hepatic vein, the swelling of the liver and spleen, the congestion of the mesentery, the enlargement of the abdominal vein and portal vein, and significantly elevated portal vein pressure [group A: (10.00±0.38) mmHg(1 mmHg=0.133 kPa); group B: (15.50±0.59) mmHg; group C: (17.25±0.48) mmHg, P=0.016], reduced the balloon degeneration of liver cell (P=0.007). As compared with the saline group (2.80±0.38), the collateral vessel angiogenesis was significantly increased in the liver and esophagus and gastric fundus (8.20±0.53, P=0.000). Portal vein pressure reduced, and ascites decreased, the balloon degeneration of liver cells, and liver and spleen congestion (P=0.028) alleviated in the VEGF group. Conclusion VEGF can improve the portal hypertension in B-CS rats by promoting angiogenesis in the medial and lateral branches of the liver. Key words: Budd-Chiari syndrome; Portal hypertension; Vascular endothelial growth factor