The outcome of defibrillation shocks is determined by the nonlinear transmembrane potential response (Vm) induced by strong external electrical field in cardiac cells. We investigated contribution of electroporation to Vm transients during high-intensity shocks using optical mapping. Rectangular and ramp stimuli (10-20 ms) of different polarities and intensities were applied to the rabbit heart epicardium during plateau phase of the action potential. Vm were optically recorded under the custom 6-mm-diameter electrode using voltage-sensitive dye. Gradual increase of cathodal and well as anodal stimulus strength was associated with: a) saturation and subsequent reduction of Vm; b) post-shock diastolic resting potential (RP) elevation, c) post-shock action potential amplitude (APA) reduction. Weak stimuli induced monotonic Vm response and did not affect RP level. Strong shocks produced non-monotonic Vm response, caused RP elevation and reduction of post-shock APA. The maximum positive and maximum negative Vm were recorded at 170±20 mA/cm² for cathodal and at 240±30 mA/cm² for anodal stimuli, respectively (mean ± SEM, n=8, p=0.003). RP elevation reached 10% of APA at stimulus strength 320±40 mA/cm² for both polarities. Strong ramp stimuli (20 ms 600 mA/cm²) induced non-monotonic Vm response, reaching the same largest positive and negative values as for rectangular shocks. Transition from monotonic to non-monotonic morphology correlates with RP elevation and APA reduction, which is consistent with cell membrane electroporation. Strong shocks resulted in Propidium Iodide uptake, suggesting sarcolemma electroporation. Conclusions: Electroporation is a likely explanation of the saturation and non-monotonic nature of cellular responses reported for strong electric stimuli.