THE CARDIAC IRREGULARITIES PRODUCED BY EPHEDRINE AND A PROTECTIVE ACTION OF SODIUM BARBITAL

• Published in: The Journal of pharmacology and experimental therapeutics Vol. 51; no. 3; p. 287
• Main Authors: WALTER J. MEEK, M. H. SEEVERS
• Format: Journal Article
• Language: English
• Published: American Society for Pharmacology and Experimental Therapeutics 01.07.1934
• ISSN: 0022-3565; 1521-0103

The effect of ephedrine on cardiac rhythm has been recorded by the electrocardiograph after intravenous injection of the drug into intact dogs. Doses of 0.5 to 6 or 8 mgm. per kilogram produce almost at once a stage of marked bradycardia. This more or less quickly merges into a second stage characterized by ectopic extrasystoles and slow ectopic rhythms. These two stages are believed to be largely the result of reflex vagal stimulation from the high blood pressure. The first is a direct inhibition of the normal pacemaker. The second consists of escape phenomena from the lower automatic centers. Coincident with the escape phenomena there is developing a third stage of excitation. This is shown by the slow rhythms occasionally passing into tachycardias. If ephedrine is given after atropin the reflex effects are eliminated and the stage of stimulation is reached almost at once, tachycardias being observed in almost every experiment. Ephedrine also affects cardiac conduction. In stage two there are various types of block due to reflex vagal stimulation. In the third stage of excitation bundle branch block and disturbed ventricular conduction are probably caused by the opening up of abnormal pathways. Doses from 6 to 20 mgm. per kilogram of ephedrine begin to show a fourth stage of depression. As the amount injected is raised above 20 mgm. paralysis of the upper automatic centers begins to occur and the ventricle may pass into fibrillation. After 125 to 200 mgm. per kilogram of sodium barbital there is a high degree of protection against the cardiac effects of ephedrine. Since barbital somewhat increased the normal heart rate, but slows it after atropine, it is believed the protection is brought about by a certain degree of vagal paralysis and a simultaneous depression of the automatic centers.