Chronic Bile Duct Ligation in the Dog: Hemodynamic Characterization of a Portal Hypertensive Model

Authors

  • Jaime Bosch,

    1. Hepatic Hemodynamics Laboratory and Departments of Surgery and Pathology, West Haven Veterans Administration Medical Center and Yale University School of Medicine, New Haven, Connecticut 06516
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    • Dr. Bosch was supported in part by a grant from the Institute Nacional de la Salud, Spain.

    • Dr. Bosch was also the recipient of a sabbatical leave from the Hospital Clinico y Provincial and University of Barcelona School of Medicine, Barcelona, Spain

  • Rosa Enriquez,

    1. Hepatic Hemodynamics Laboratory and Departments of Surgery and Pathology, West Haven Veterans Administration Medical Center and Yale University School of Medicine, New Haven, Connecticut 06516
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  • Roberto J. Groszmann,

    Corresponding author
    1. Hepatic Hemodynamics Laboratory and Departments of Surgery and Pathology, West Haven Veterans Administration Medical Center and Yale University School of Medicine, New Haven, Connecticut 06516
    • Roberto J. Groszmann, M.D., Hepatic Hemodynamics Laboratory, Veterans Administration Medical Center, West Spring Street, West Haven, Connecticut 06516.
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  • Edward H. Storer

    1. Hepatic Hemodynamics Laboratory and Departments of Surgery and Pathology, West Haven Veterans Administration Medical Center and Yale University School of Medicine, New Haven, Connecticut 06516
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Abstract

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 (110 ± 4 mm Hg vs. normal 136 ± 6 mm Hg; p < 0.005) and peripheral vascular resistance (4.60 ± 0.38 vs. 6.28 ± 0.38 dynes-sec-cm−5; p < 0.02), and an increase in cardiac index (129 ± 7 vs. 98 ± 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 ± 0.6 mm Hg vs. 6.7 ± 0.5 mm Hg; p < 001) and wedged hepatic venous pressure (14 ± 1.2 mm Hg), the development of extensive portal-systemic shunting (49 ± 10 vs. 0.03 ± 0.017c; p < 0.01), and a decrease in portal venous flow (194 ± 21 ml per min vs. 427 ± 21 ml per min; p < 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.

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