oxyfedrine and Arrhythmias--Cardiac

The effects of alifedrine, a positive inotropic agent, were examined in greyhounds anaesthetised with chloralose. An intravenous dose of 0.3 mg kg-1 resulted in a substantial increase in myocardial contractility (increased dP/dtmax, cardiac output and stroke volume) without significantly affecting heart rate. The effects of alifedrine on the severity of arrhythmias resulting from both coronary artery occlusion and reperfusion were also determined. A mild antiarrhythmic effect was observed during early ischaemia when the incidence of ventricular tachycardia was reduced from 90% in controls to 50% in treated dogs. There was also a significant reduction in the number of extrasystoles appearing as ventricular tachycardia (from 511 +/- 138 to 151 +/- 84). The total number of extrasystoles during the first 30 min of ischaemia was also reduced, although not significantly, from 846 +/- 193 to 527 +/- 86. Following release of a 40 min coronary artery occlusion there was a marked reduction in reperfusion-induced ventricular fibrillation from 75% in controls, to 37% in the alifedrine-treated dogs. The overall survival from the combined occlusion-reperfusion insult was increased from 20% in controls to 50%. These results suggest that alifedrine has an unusual and useful spectrum of pharmacological activity in that it combines antiarrhythmic activity with an ability to improve cardiac function.

Topics: Animals; Arrhythmias, Cardiac; Cardiotonic Agents; Coronary Circulation; Coronary Disease; Dogs; Female; Hemodynamics; Male; Oxyfedrine; Propiophenones

In 20 patients the electrophysiologic effects of oxyfedrine at doses of 0.3 mg/kg/hr and 0.6 mg/kg/hr were studied. At the low dose, oxyfedrine caused a significant shortening of the absolute and rate-corrected sinus node recovery time by 16 and 27 percent, respectively. Sinus cycle length decreased slightly by 9 percent. Estimated sinoatrial conduction time tended to shorten, but not significantly so. AV-nodal conduction was slightly accelerated at sinus rhythm as well as during atrial stimulation; correspondingly paced cycle length at which Wenckebach AH-conduction occurred decreased. HV-interval remained unchanged. Increasing the dose of oxyfedrine had no additional effect on electrophysiologic parameters compared to the first dose used. The results demonstrate a moderate stimulatory action of oxyfedrine on sinus nodal automaticity and a slight acceleration of AV-nodal conduction. Whether the drug might be useful in the clinical setting for medical management of sinus nodal dysfunction or AV-conduction disturbances, remains to be elucidated on long-term studies; more pronounced effects of oxyfedrine than found in this investigation, however, are expected to be limited by its autoinhibitory action at higher dose levels.

Topics: Adult; Aged; Arrhythmias, Cardiac; Atrioventricular Node; Dose-Response Relationship, Drug; Electrocardiography; Female; Heart Conduction System; Heart Rate; Humans; Male; Middle Aged; Oxyfedrine; Propiophenones; Sinoatrial Node; Syncope

Topics: Animals; Arrhythmias, Cardiac; Coronary Circulation; Coronary Disease; Hemodynamics; In Vitro Techniques; Lactates; Myocardium; Oxyfedrine; Propiophenones; Swine

Topics: Adult; Aged; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Atrial Fibrillation; Bradycardia; Drug Evaluation; Female; Heart Block; Heart Conduction System; Humans; Male; Middle Aged; Oxyfedrine; Propiophenones

Topics: Adolescent; Adult; Aged; Arrhythmias, Cardiac; Bundle of His; Child; Electrocardiography; Female; Heart Conduction System; Humans; Male; Middle Aged; Oxyfedrine; Propiophenones; Stimulation, Chemical