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1 Department of Physiology, School of Veterinary Medicine of Hannover, 30173 Hannover, Germany; and 2 Department of Biomedical Engineering, The Johns Hopkins University, Baltimore, Maryland 21205
Cardiac tissue dysfunction can result from
high-intensity electrical shocks and is manifested as changes in
transmembrane potential
(Vm).
Ten-millisecond shock pulses (SPs) of varying intensity and polarity
were applied to frog ventricle in diastole, and
Vm 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. APAs
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
APAs was marginally significant 1 s after SP delivery (P = 0.063). The
peak change in Vm
during 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.
cardiac tissue; voltage-sensitive dye; anodal shock; cathodal shock; extracellular electrode; electroporation
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