Glucagon selectively increases splanchnic blood flow in patients with well-compensated cirrhosis

Authors

  • Dr. Samuel S. Lee,

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

  • Richard Moreau,

    1. Unité de Recherches de Physiopathologie Hépatique, INSERM U 24, Hǒpital Beaujon, Clichy, France
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  • Dr. Antoine Hadengue,

    1. Unité de Recherches de Physiopathologie Hépatique, INSERM U 24, Hǒpital Beaujon, Clichy, France
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    • Drs. Hadengue and Koshy were supported by the Fondation pour la Recherche Médicale.

  • Raimondo Cerini,

    1. Unité de Recherches de Physiopathologie Hépatique, INSERM U 24, Hǒpital Beaujon, Clichy, France
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  • Abraham Koshy,

    1. Unité de Recherches de Physiopathologie Hépatique, INSERM U 24, Hǒpital Beaujon, Clichy, France
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  • Dr. Didier Lebrec

    Corresponding author
    1. Unité de Recherches de Physiopathologie Hépatique, INSERM U 24, Hǒpital Beaujon, Clichy, France
    • INSERM U 24, Hǒpital Beaujon, 92118 Clichy, France
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Abstract

To delineate the circulatory effects of glucagon in cirrhosis, we infused two moderately supraphysiological doses of this hormone into 19 patients with cirrhosis and determined hemodynamic responses. Patients were divided into a group with good liver function (Pugh Class A, n = 8) and poorer function (Pugh Class B and C, n = 11). All patients received glucagon at 10 ng per kg per min for 20 min, then 20 ng per kg per min for a further 20 min. These doses raised serum glucagon levels to a similar degree in both groups of patients. Serum glucose levels also rose in both groups but to a lesser degree in Class BC patients. Serum noradrenaline and adrenaline remained unchanged in both groups. Heart rate, mean arterial pressure, cardiac index, systemic vascular resistance, hepatic venous pressure gradient and hepatic blood flow were measured basally and during the second glucagon infusion. None of these measurements significantly changed in either group of patients. Azygos and renal venous blood flow were measured basally and during the first and second infusions. Azygos flow increased significantly only in Group A patients: basal, 0.32 ± 0.03 liter per min; first infusion, 0.40 ± 0.06 liter per min; second infusion, 0.49 ± 0.07 liter per min. Corresponding values in Group BC patients were: 0.54 ± 0.08, 0.54 ± 0.08 and 0.52 ± 0.08 liter per min. Renal blood flow did not change significantly. One patient with a portacaval shunt increased superior mesenteric venous flow from 0.78 liter per min to 0.95 liter per min with glucagon. These results, showing a selective increase in superior portocollateral flow in well-compensated patients, suggest that glucagon can act as a splanchnic vasodilator. However, since progression of liver disease was associated with attenuation of this response, we suggest that glucagon may mediate splanchnic hyperemia only in the early stages of cirrhosis.

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