Cardiopulmonary arrest and resuscitation produces a tremendous physiological stress with resultant biochemical derangements. Previous research has shown that infusion of glucose, insulin, and potassium improves myocardial function during ischemia. The purpose of this investigation was to determine insulin and glucose levels during cardiopulmonary arrest in the canine model. Baseline insulin and glucose levels were obtained from an ascending aortic arch catheter in 6 adult mongrel dogs. Ventricular fibrillation was induced by an electrical stimulus and ventilation was terminated. After 5 rain of fibrillation, CPR was initiated using external, mechanical CPR and a continuous epinephrine infusion at 5 t~g/kg/min. Serum insulin and glucose levels were repeated 15 min after beginning CPR. Mean serum glucose 15 min after initiation of resuscitation (305 + 114 mg/dL) was significantly increased from prearrest levels {124 +_ 29 mg/ dL, P < .01). Mean serum insulin 15 rain after initiation of resuscitation (11.3 ยฑ 3.3 I~U/mL} was significantly decreased compared to prearrest levels (16.2 ยฑ 6.0 I~U/mL, P < .05). Epi-nephrine, because of its ~-sympathetic activity, suppresses insulin release from the pancreas and inhibits the net effect of insulin at the insulin receptor. During ischemia, the myocardium becomes primarily dependent on glucose as a source of energy. Inappropriately low insulin levels during CPR may adversely affect an already compromised myocardial glucose metabolism. Further investigation is needed to determine the utility of insulin infusion during CPR.