In an attempt to elucidate the genesis of bifid T waves, we recorded transmembrane potentials of subepicardial ventricular muscle fibers simultaneously with a bipolar ventricular electrogram in isolated, perfused rabbit hearts, and the timing of the two apices of the T wave (aT1, aT2) was correlated with ventricular repolarization. The following results were obtained. (1) In seven of the nine hearts in which the repolarization process was mapped on the anterior and posterior surfaces of both ventricles, the 80% repolarization times of the left and the right ventricles were scattered around aT1 and aT2, respectively, and their average values closely corresponded to Q-aT1 and Q-aT2 intervals. This suggested that aT1 and aT2 depended on repolarization of the left and the right ventricles, respectively. (2) In one heart, aT1 appeared to reflect repolarization of the posterior ventricular wall, and aT2 that of the anterior wall. (3) In the remaining heart, aT2 coincided with repolarization of the anterobasal portion of the right ventricle, and aT1 that of the remaining portions of the ventricles. Even when ventricular repolarization was modified by low K+, low Ca2+ or procainamide perfusion, or by premature atrial stimulation, the close temporal correlation of the left and right ventricular repolarization with the two apices of the T wave was maintained. Selective cooling of the perfusate in either the left or the right coronary artery resulted in the production of bifid T waves in which aT2 coincided with the delayed repolarization of the cooled ventricle. We conclude that either physiologically or pathologically delayed repolarization in certain portions of the ventricles is most likely the cause of bifid T waves.