Effects of Alpha and Beta Adrenergic Blocking Agents on Cyclopropane-Catecholamine Cardiac Arrhythmias

Open Access
Publisher Website
Google Scholar
Abstract
Cardiac arrhythmias were produced in the cat by the injection of epinephine, norepinephine, ethyl-norepinephine or isoproterenol during the inhalation of 25% cyclopropane in oxygen. The injection of dibenamine, an alpha adrenergic blocking agent, produced epinephrine reversal, decreased the pressor response to norepinephrine and increased the depressor response to isoproterenol. Dibenamine did not consistently increase the threshold doses of catecholamines required to produce cardiac arrhythmias. In those instances where the arrhythmia threshold doses of the catecholamines were increased, usually to twice control, this result often was attributable to a modification by dibenamine of the pressor effects of the catecholamines. The beta adrenergic blocking agent proethalol produced ethylnorepinephrine reversal, increased the pressor response to epinephine and markedly reduced or abolished the depressor response to isoproterenol. The arrhythmia threshold doses of the catecholamines were increased to 8 times those of controls. Large doses of isoproterenol (3 mg/kg) produced beta adrenergic blockade and increased the arrhythmia threshold doses of the catecholamines to 4 times those of controls. The results suggest that cyclopropane-catecholamene arrhythmias are blocked by specific beta adrenergic blockade and that myo-cardial ectopic excitation may be attributable to the beta adrenergic receptors.