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 (APA(s)) decreased sigmoidally toward 75-85% of the control AP amplitude (APA(c)) and zero, respectively. APA(s) was 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 APA(s) was marginally significant 1 s after SP delivery (P = 0.063). The peak change in V(m) during SP (across all intensity levels) was -200% APA(c) for anodal and +125% APA(c) for cathodal pulses. In conclusion, we show that SP reduces APA in a sigmoidal fashion at strengths >10-20 x diastolic threshold and is more deleterious for anodal polarities.