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July 1973

Glucagon Infusion Following Phosphodiesterase InhibitionAn Experimental Study of the Hemodynamic Effects

Author Affiliations

Loma Linda, Calif
From the Surgical Research Laboratory, Loma Linda University School of Medicine, Loma Linda, Calif.

Arch Surg. 1973;107(1):12-15. doi:10.1001/archsurg.1973.01350190004002

The hemodynamic effects of a potent phosphodiesterase inhibitor (PDI), 3-bromo-5,7-dimethylpyrazolo(1,5a)pyrimidine, have been studied in a group of 18 dogs. Glucagon alone was compared to glucagon and PDI infusions. Control animals received saline only in a volume equal to that employed in the treated groups. The phosphodiesterase inhibitor was found to potentiate the rise in cardiac output when added before and during the glucagon infusion by an average of 57% (P<.01) over that observed with glucagon and saline. Glucagon and PDI together increased the cardiac output by 120% (P <.001) above that observed in the saline controls. The phosphodiesterase inhibitor caused no significant change in arterial pressure, heart rate, central venous pressure, or hematocrit reading. It consistently decreased peripheral resistance. These findings provide additional evidence that the cardiovascular effects of glucagon are mediated by cyclic 3′,5′-adenosine monophosphate. The potentiation of glucagon by PDI raises the possibility of its use in the clinical management of certain low perfusion states.