Epinephrine is thought to improve the success of defibrillation with countershock therapy. However, a recent study failed to show any effect of epinephrine in dogs with normal coronary arteries undergoing electrically-induced ventricular fibrillation (VF). In the current study, the effects of epinephrine were examined in dogs with coronary occlusion undergoing both spontaneous and electrically-induced fibrillation. Forty pentobarbital-anesthetized dogs were prepared by placing snares around the circumflex and left anterior descending coronary arteries. Fibrillation and subsequent resuscitation were carried out with one coronary artery occluded. Dogs were randomly allocated so that half of the animals underwent spontaneous fibrillation and half were electrically fibrillated. In addition, half received epinephrine (1 mg) during resuscitation and half received normal saline solution (1 ml). After 3 minutes of cardiac arrest, cardiopulmonary resuscitation (CPR) was begun, and 30 seconds later epinephrine or saline were injected. One minute later defibrillation was attempted using successive stored energy doses of 1, 2, 4, 8, 16, and 32 J/kg. Delivered energy and transthoracic impedance were measured for each countershock. Successful defibrillation was defined as conversion to any rhythm other than VF or ventricular tachycardia that degenerated in VF within 10 seconds. No other drugs were given during resuscitation. Neither the type of fibrillation (electrically-induced versus spontaneous) or drug therapy (epinephrine versus placebo) had a significant effect on the incidence of defibrillation or the energy necessary for successful defibrillation. Epinephrine did significantly increase the incidence of resuscitation.(ABSTRACT TRUNCATED AT 250 WORDS)