Effects of Arterial Hypoxemia and Splenic Nerve Stimulation on Myocardial Adenosine 3,5’-Monophosphate in Dogs

Abstract

Epinephrine infusion, 5-percent oxygen breathing, and splenic nerve stimulation were employed to increase cardiac output by 50–100 % in anesthetized dogs. Epinephrine infusion, as expected, increased plasma and myocardial cyclic AMP concentrations. Arterial hypoxemia increased cyclic AMP concentration in plasma but not in the heart. Practolol pretreatment abolished the increase in plasma cyclic AMP concentration and reduced the rise in cardiac output during hypoxemia. Splenic nerve stimulation was not associated with increases in either plasma or myocardial cyclic AMP. Adenylate cyclase activity was increased by addition of plasma into the incubation medium. However, splenic venous plasma obtained during splenic nerve stimulation did not increase adenylate cyclase activity more than control plasma obtained before stimulation. We conclude that the positive inotropic action of arterial hypoxemia and splenic nerve stimulation does not depend on the adenylate cyclase-cyclic AMP system.

Myocardial extraction of cyclic AMP during pacing-induced angina

“…Reports have been made concerning the release of cyclic AMP from cells into extracellular fluids in response to exogenous epinephrine, glucagon and parathyreoid hormone (16-18) and increased plasma cyclic-AMP levels in arterial hypoxemia (19). Cyclic AMP mediates the glycogenolytic (5-7) and lipolytic response (1) of catecholamines and glucagon.…”