AJP - Gastrointestinal and Liver Physiology, Vol 251, Issue 5 674-G677, Copyright © 1986 by American Physiological Society
Role of glucagon in splanchnic hyperemia of chronic portal hypertension
J. N. Benoit, B. Zimmerman, A. J. Premen, V. L. Go and D. N. Granger
The role of glucagon as a blood-borne mediator of the hyperdynamic
circulation associated with chronic portal venous hypertension was assessed
in the rat portal vein stenosis model. Selective removal of pancreatic
glucagon from the circulation was achieved by intravenous infusion of a
highly specific glucagon antiserum. Blood flow to splanchnic organs,
kidneys, and testicles was measured with radioactive microspheres, and the
reference-sample method. Glucagon antiserum had no effect on blood flow in
the gastrointestinal tract of sham-operated (control) rats. However, the
antiserum produced a significant reduction in hepatic arterial blood flow
in the control rats, suggesting that glucagon contributes significantly to
the basal tone of hepatic arterioles. In portal hypertensive rats glucagon
antiserum significantly reduced blood flow to the stomach (22%), duodenum
(25%), jejunum (24%), ileum (26%), cecum (27%), and colon (26%). Portal
venous blood flow was reduced by approximately 30%. The results of this
study support the hypothesis that glucagon mediates a portion of the
splanchnic hyperemia associated with chronic portal hypertension.
