Lack of vasopressin action on splanchnic hemodynamics during bleeding: A study in conscious, portal hypertensive rats

Authors

  • Dr. Dominique Valla,

    Corresponding author
    1. Unite de Recherches de Physiopathologie Hépatique (INSERM U 24), Hǒpital Beaujon, 92118 Clichy, France
    • INSERM U 24, Hǒpital Beaujon, 92118 Clichy, France
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  • Catherine Girod,

    1. Unite de Recherches de Physiopathologie Hépatique (INSERM U 24), Hǒpital Beaujon, 92118 Clichy, France
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  • Samuel S. Lee,

    1. Unite de Recherches de Physiopathologie Hépatique (INSERM U 24), Hǒpital Beaujon, 92118 Clichy, France
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    • Dr. Lee was supported by a fellowship from the Medical Research Council of Canada.

  • Alain Braillon,

    1. Unite de Recherches de Physiopathologie Hépatique (INSERM U 24), Hǒpital Beaujon, 92118 Clichy, France
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  • Didier Lebrec

    1. Unite de Recherches de Physiopathologie Hépatique (INSERM U 24), Hǒpital Beaujon, 92118 Clichy, France
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Abstract

Due to the marked effects of hemorrhage on cardiac output and splanchnic hemodynamics, the circulatory actions of vasopressin may differ during bleeding as opposed to stable conditions. We evaluated this hypothesis in conscious rats with portal hypertension due to chronic portal vein stenosis, by comparing the effects of a vasopressin infusion (0.02 IU per kg per min) to those of a control saline infusion, during and after a hypoten-sive hemorrhage (25 ml per kg). We also studied unbled portal hypertensive rats receiving an identical infusion of vasopressin or saline. During and after hemorrhage, vasopressin induced significant changes in systemic hemodynamics but had no effect on portal pressure, portal tributary blood flow and nonhepatic splanchnic arteriolar resistance. In unbled animals, by contrast, vasopressin decreased portal pressure and portal tributary blood flow and increased nonhepatic splanchnic arteriolar resistance. Our data further indicate that hemorrhage alone caused an early vasoconstriction in the portal tributaries and a delayed vasoconstriction in the nonsplanchnic vascular bed while vasopressin during hemorrhage induced an early and sustained vasoconstriction in the nonsplanchnic vascular bed as well as in the portal tributaries. The results show that, during and after severe bleeding, vasopressin exerts little influence on portal hemodynamics. Although these data do not allow firm conclusions concerning the therapeutic efficacy of vasopressin in bleeding esophageal varices, they demonstrate that the splanchnic actions of vasoac-tive substances cannot be readily extrapolated from stable conditions to hemorrhage.

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