Bipolar potentials were recorded from intramural electrodes located within areas of acute myocardial ischemia in dogs. Alterations in bipolar potential electromotive force (EMF) and local activation times were measured at predetermined intervals up to 12 hours after coronary occlusion. Histochemical stains were used to correlate structural biochemical changes with sites of electrophysiologic changes. In severely ischemic areas, bipolar potentials lost 50% of their preocclusion EMF within 30 min and 95% within 6 hours at which time all parameters stabilized. Lesser decreases in bipolar potential EMF were recorded in the peripheral areas of the infarct. Bipolar potential EMF increased at the junction of ischemic and normal myocardium. Activation time was delayed in ischemic areas but no correlation between the magnitude of delay and the degree of tissue ischemia could be established. Coronary reperfusion after 30 min, 1 hr, 2 hr and 6 hr of occlusion resulted in some return in bipolar potential EMF, decreasing as a function of duration between occlusion and reperfusion. Variation in the degree of ischemia of different zones of injury within an acute myocardial infarction, as well as a different response of those zones to the return of blood flow, was shown.