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Original communication| Volume 81, ISSUE 3, P326-334, March 1977

Adrenergic mechanisms in the hepatic arterial circulation of baboons

  • Kenneth G. Swan
    Correspondence
    Reprint requests: Kenneth G. Swan, M.D., Director, Division of General and Vascular Surgery, New Jersey Medical School, 100 Bergen St., Newark, N.J. 07103.
    Affiliations
    From the Department of Surgery, College of Medicine and Dentistry of New Jersey, New Jersey Medical School, Newark, N. J., USA

    From the Division of Surgery, Walter Reed Army Institute of Research, Walter Reed Army Medical Center, Washington, D. C. USA
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  • John C. Kerr
    Affiliations
    From the Department of Surgery, College of Medicine and Dentistry of New Jersey, New Jersey Medical School, Newark, N. J., USA

    From the Division of Surgery, Walter Reed Army Institute of Research, Walter Reed Army Medical Center, Washington, D. C. USA
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  • Creighton B. Wright
    Affiliations
    From the Department of Surgery, College of Medicine and Dentistry of New Jersey, New Jersey Medical School, Newark, N. J., USA

    From the Division of Surgery, Walter Reed Army Institute of Research, Walter Reed Army Medical Center, Washington, D. C. USA
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  • David G. Reynolds
    Affiliations
    From the Department of Surgery, College of Medicine and Dentistry of New Jersey, New Jersey Medical School, Newark, N. J., USA

    From the Division of Surgery, Walter Reed Army Institute of Research, Walter Reed Army Medical Center, Washington, D. C. USA
    Search for articles by this author
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      Abstract

      The effects of intra-arterial injections and infusions of three adrenergic amines upon hepatic arterial blood flow were measured in anesthetized baboons before and after alpha and beta adrenergic blockade with intravenous phenoxybenzamine and propranolol. Injections of norepinephrine or epinephrine caused dose-dependent decreases in hepatic arterial blood flow. These responses were attenuated by alpha adrenergic blockade and were unchanged by beta adrenergic blockade. Injections of isoproterenol caused dose-dependent increases in hepatic arterial flow. These increases were relatively small and were reversed to constriction at low doses and attenuated at high doses of the agonist by beta adrenergic blockade. Intrahepatic arterial infusions of constrictors were unaccompanied by autoregulatory excape. The degree of constriction was attenuated by alpha adrenergic blockade but was not potentiated by beta adrenergic blockade. Intrahepatic arterial infusion of a relatively large dose of isoproterenol was required to evoke a relatively modest, but sustained, increase in hepatic arterial blood flow. This response was not potentiated by alpha adrenergic antagonism, but was attenuated by beta adrenergic blockade. These observations suggest an apparent and relative decrease in beta adrenergic receptor activity in the hepatic arterial bed of the baboon when compared to other regional circulations such as the mesenteric and femoral beds. These beta receptors are relatively resistant to both stimulation and blockade.
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