THERE IS a great deal of evidence suggesting that the most frequent mechanism of death in coronary occlusion is by ventricular fibrillation. Very often this fatal complication may occur following small infarcts which apart from the acute arrhythmia, would have permitted survival with adequate myocardial function. A number of investigators have observed that a larger incidence of ventricular fibrillation occurs in the first 5-20 minutes following the production of the occlusion; thereafter the incidence decreases considerably. Although the pathogenesis of the ventricular fibrillation in coronary occlusion is not completely understood, it is believed that early and late fibrillation differ in the mechanism of their production. This study was carried out to ascertain the role of localized anoxia as a trigger mechanism in early ventricular fibrillation following coronary artery occlusion.For this purpose the artery distal to the occlusion was perfused with a nonoxygenated medium in order to eliminate the stasis which