Splanchnic and systemic hemodynamics were measured in six normal dogs and in 18 dogs that had the bile ducts ligated for a period of 8 weeks. In the bile duct-ligated dogs, there was a decrease in arterial pressure (1 10 f 4 mm Hg vs. normal 136 f 6 mm Hg; p < 0.005) and peripheral vascular resistance (4.60 f 0.38 vs. 6.28 f 0.38 d~nes-sec-crn-~; p c 0.02), and an increase in cardiac index (129 f 7 vs. 98 f 9 ml per min per kg; p < 0.05). The splanchnic hemodynamic characteristics in the bile duct-ligated dogs included an increase in portal venous pressure (13.3 f 0.6 mm Hg vs. 6.7 f 0.5 mm Hg; p c 001) and wedged hepatic venous pressure (14 f 1.2 mm Hg), the development of extensive portal-systemic shunting (49 f 10 vs. 0.03 f 0.01%; p c 0.01), and a decrease in portal venous flow (194 f 21 ml per min vs. 427 f 21 ml per min; p c 0.001). This study demonstrated that chronic bile duct-ligated dogs develop sinusoidal portal hypertension with extensive portal-systemic shunting and a hyperdynamic systemic circulation. These findings closely resembled hemodynamic abnormalities observed in human cirrhosis and suggest that this model is useful in physiopathological and pharmacological studies of portal hypertension.
Chronic bile duct ligation (CBDL) in the dog is used as an animal model of ascites in liver disease (1-6). This dog model has been shown to develop significant increments in portal venous pressure and to have functional renal abnormalities similar to those observed in cirrhotic patients. Corrosion cast studies in the CBDL dog have shown a marked distortion of the liver vascular architecture (1). In addition, large venous collaterals were observed in dogs 3 to 4 months after CBDL (7-9).
The present work was designed to study the systemic and splanchnic hemodynamic abnormalities in this animal model. Our results demonstrate that CBDL in the dog is a reliable model of intrahepatic portal hypertension with extensive portal-systemic shunting (PSS). The similarities in the portal and systemic hemodynamic