AJP - Heart and Circulatory Physiology, Vol 253, Issue 2 480-H486, Copyright © 1987 by American Physiological Society
Microlesion formation in myocardial cells by high-intensity electric field stimulation
J. L. Jones, R. E. Jones and G. Balasky
Arrhythmias, S-T segment changes, immediate refibrillation, and other signs
of dysfunction are often observed after clinical and experimental
transthoracic defibrillation. In vitro studies suggested that shock-induced
dysfunction is induced by sarcolemmal dielectric breakdown accompanied by
ionic exchanges through transient, shock-induced microlesions in the
sarcolemma. To test this hypothesis, cultured chick embryo myocardial cells
were shocked in media containing fluorescein isothiocyanate-labeled
dextrans (FITC-dextrans) ranging in molecular mass from 4 to 70 kDa, using
electric field stimulation 5 ms in duration and ranging in intensity from 0
to 200 V/cm. Results showed that the percentage of cells incorporating 4-
to 20-kDa dextrans increased in a dose-dependent manner. The 4- and 10-kDa
dextrans were incorporated beginning at intensities of 50-100 V/cm. Dextran
incorporation corresponded with shock intensities which produced a
shock-induced arrest of spontaneous contraction lasting 1 min. The 20-kDa
dextrans were incorporated following 150- and 200-V/cm shocks. Shocks of
these intensities also produced a transient postshock contracture. Larger
dextrans (40 and 70 kDa) were not incorporated. These results suggest the
formation of transient sarcolemmal microlesions having a diameter of 45-60
A during high-intensity electric field stimulation.
