RT Journal Article
SR Electronic
T1 NEUROEXCITATORY EFFECTS OF DIGITALIS AND THEIR ROLE IN THE DEVELOPMENT OF CARDIAC ARRHYTHMIAS
JF Journal of Pharmacology and Experimental Therapeutics
JO J Pharmacol Exp Ther
FD American Society for Pharmacology and Experimental Therapeutics
SP 154
OP 168
VO 183
IS 1
A1 RICHARD A. GILLIS
A1 ARTHUR RAINES
A1 YUNG J. SOHN
A1 BARRIE LEVITT
A1 FRANK G. STANDAERT
YR 1972
UL http://jpet.aspetjournals.org/content/183/1/154.abstract
AB The question of whether digitalis materials excite central nervous system structures to produce cardiorespiratory effects was evaluated in Dial-urethane-anesthetized cats. This was done by: 1) monitoring the spontaneous electrical activity in sympathetic, parasympathetic and phrenic nerves before and after ouabain administration and correlating the neural events with electrocardiographic, vascular and respiratory responses; 2) determining the influence of exclusion of the central nervous system on ouabain-induced changes in cardiac autonomic and phrenic nerve activity, ouabain-induced respiratory muscle movements and the dose of ouabain needed to produce cardiotoxicity; and 3) determining the influence of the antiarrhythmic drug propranolol on both the neural and cardiorespiratory effects of ouabain. Ouabain enhanced traffic in vagus, sympathetic and phrenic nerves; this enhancement was associated with the development of ventricular rhythm disturbances and respiratory hyperactivity. Spinal transection prevented these ouabain-induced effects and significantly increased the dose of ouabain needed to produce ventricular rhythm disorders. Administration of propranolol to animals exhibiting ouabain-induced neural augmentation usually restored neural activity to normal levels and converted the ventricular arrhythmia to a regular sinus rhythm. These data indicate that: 1) neural activation by ouabain plays a significant role in the development of cardiac arrhythmias and hyperventilation and 2) procedures which diminish neural influence (spinal section or propranolol) prevent or reverse cardiotoxicity induced by ouabain. © 1972, by The Williams & Wilkins Company