INTRODUCTION Ventricular fibrillation (VF) is an irregular@ asynchronous@ and incoordinate contractile activity of the ventricular myocardium@ and is usually a terminal cardiac event following severe myocardial infarction. VF is reversible@ and its termination can be spontaneous or can be induced by artificial means such as passing a strong electrical countershock through the heart which momentarily depresses all cardiac activity. VF can be induced artificially by several agents. The most common technique used experimentally to initiate VF is application of an electrical stimulus to the myocardium during the final stage of ventricular repolariation which is the most vulnerable period for fibrillation. The probability of VF increase with myocardial infarction. Although organic heart disease predisposes VF@ the vulnerability of the myocardium is further enhanced by myocardial ischemia. I schemia can result from a variety of causes which tend to reduce the availability of oxygen to the myocardium@ and of special interest in this investigation is the reduced carrying capacity of the hemoglobin following carbon monoxide inhalation. It was previously reported (1@2) that inhalation of carbon monoxide (100 ppm) resulted in myocardium effects in normal monkeys. And monkeys with myocardial infarction. ECG P-wave amplitudes were elevated in both groups@ and inhaling of carbon monoxide resulted in a higher incidence of T-wave inversion in infracted animals than in non-infarcted animals suggesting that there was a greater degree of myocardial ischemia in infracted animals. Since inhalation of 100 pp@ monoxide resulted in demonstrable (ECG) effects on the myocardium@ the present study was designed to determine whether carbon monoxide inhalation also influenced the susceptibility of the ventricles to fibrillation.