THE EFFECT OF SYMPATHOMIMETIC AMINES ON ARTERIAL PLASMA POTASSIUM AND CARDIAC RHYTHM IN ANESTHETIZED DOGS

¹ Department of Physiology, University of Wisconsin Medical School, Madison, Wisconsin

1. With the injection of epinephrine (0.005 mgm./kgm.) into a dog anesthetized with cyclopropane there was an abrupt rise in potassium beginning between twenty and forty seconds after the initiation of the epinephrine injection, reaching a maximum value 100 per cent above the resting level between 60 and 80 seconds and falling rapidly back to the pre-injection level by 180 seconds. Ventricular tachycardia always appeared at the time of the rapid ascent of the potassium level and extended through the peak of the rise.

2. The magnitude of the arterial plasma potassium following epinephrine administration cannot alone account for differences in cardiac response seen when a dog is unanesthetized or anesthetized with cyclopropane or sodium pentobarbital since there is considerable rise in potassium in all cases but ventricular tachycardia only during cyclopropane anesthesia.

3. Ventricular tachycardia that can be produced during cyclopropane anesthesia is not always accompanied by a marked increase in arterial potassium since Aranthol is capable of producing this arrhythmia with only a slight potassium rise.

4. Ephedrine and Neosynephrine produce considerably less potassium rise than equipressor doses of epinephrine during cyclopropane anesthesia and usually they fail to produce ventricular tachycardia.

5. DHE-45 and Dibenamine not only protect against cyclopropane-epinephrine ventricular tachycardia but also markedly inhibit the potassium response to epinephrine.