Microlesion formation in myocardial cells by high-intensity electric field stimulation

Abstract

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.

Low K+‐induced hyperpolarizations trigger transient depolarizations and action potentials in rabbit ventricular myocytes

“…Cell membrane ruptures produced by electroporation have large pores allowing permeation of large molecules and, therefore, are not selective for any particular organic and inorganic ions (Jones et al 1987;Teruel & Meyer, 1997). The fact that low [K¤]ï activated irregular depolarizations and inward currents in the presence of both NMDG and aspartate is consistent with the non-selective nature of the conductance induced by hyperpolarization.…”

Nonlinear Changes of Transmembrane Potential During Electrical Shocks

“…23 In multicellular preparations, electroporation can be detected by observing uptake of a membraneimpermeable dye. 24 In several studies, 16,17 elevation of diastolic potential was used as a sign of membrane electroporation, but no study until now has established a causative link between the two phenomena using direct measurements of electroporation. Therefore, mechanisms other than electroporation contributing to diastolic V m elevation after shocks could not be excluded.…”

Role of peak current in conversion of patients with ventricular fibrillation

“…Some of the highest peak currents in this study were used in patients with low TTI. This is of concern, as the very high peak currents generated may result in the formation of membrane microlesions at the regions of high current density, (33) which would increase the chance of post-shock myocardial dysfunction. This suggests that high-current shocks should be avoided, especially in low TTI patients, to reduce the chances of myocardial damage.…”