We have investigated the effects of electric field stimulation on membrane repolarization in rabbit papillary muscles and assessed the consequences of these effects for the dispersion of intracellular potentials and the production of a propagation wave front or unidirectional block in relatively refractory tissue. The stimuli studied had electric field strength of 0.25–14 V/cm, duration of 2 msec, and field orientation along or across the myocardial fibers. The field strengths to excite the muscles in diastole were 0.68 or 1.23 V/cm for stimuli oriented along or across the fibers, respectively (p<0.01, along versus across). A 2.5-V/cm stimulus given near the end of the action potential (AP) produced either no response or, after increasing the stimulus delay only 2–3 msec, a full response with almost no AP durations that were intermediate. For stimulation along and across the fibers, respectively, given at 70% of the AP duration, a 4-V/cm stimulus produced AP prolongation (measured at 90% repolarization) of 209%, and 4% (p<0.05), an 8-V/cm stimulus produced AP prolongation of 36% and 20% (p<0.05), and a 14-V/cm stimulus produced AP prolongation of 36% and 30% (p=NS). For either orientation, AP prolongation by stimuli of 8 V/cm or 14 V/cm increased gradually as the stimulus delay was increased. The different effects in relatively refractory tissue of stimuli of 2.5 V/cm compared with 8 V/cm can explain the propagation wave front and block that occur with electrically induced functional reentry in the heart. After stimulation with fields below a critical strength (∼5 V/cm), a large intracellular potential difference may occur among cells that are sufficiently recovered to become excited by the stimulus and cells that are not sufficiently recovered to become excited, consistent with the reported propagation wave front where the two groups of cells are closely opposed. After stimulation with fields above the critical strength, differences in intracellular potentials among cells during repolarization may be decreased, and the intracellular potentials may be in a range in which sodium current is inactivated, consistent with the reported absence of a propagation wave front. Thus, the different effects of low and high electric field strengths can account for the “critical point” mechanism for unidirectional block and reentry.