Dose-dependent reduction of cardiac transmembrane potential by high-intensity electrical shocks.

Cardiac tissue dysfunction can result from high-intensity electrical shocks and is manifested as changes in transmembrane potential ( V m). Ten-millisecond shock pulses (SPs) of varying intensity and polarity were applied to frog ventricle in diastole, and V m was quantified directly under the stimulating electrode by an optical method using voltage-sensitive dye. As SP intensities were increased, the shock-induced action potential (AP) plateau and AP amplitude (APAs) decreased sigmoidally toward 75-85% of the control AP amplitude (APAc) and zero, respectively. APAswas shifted toward lower current densities for anodal compared with cathodal SPs (half-maximal values 185 and 238 mA/cm2, respectively; P = 0.02). Recovery of APAs was marginally significant 1 s after SP delivery ( P = 0.063). The peak change in V mduring SP (across all intensity levels) was -200% APAc for anodal and +125% APAc for cathodal pulses. In conclusion, we show that SP reduces APA in a sigmoidal fashion at strengths >10-20 × diastolic threshold and is more deleterious for anodal polarities.