Electroporation and recovery of cardiac cell membrane with rectangular voltage pulses

Abstract

Electroporation of the cardiac cell membrane may result from intense electric fields applied to cardiac muscle, associated for example with defibrillation and cardioversion. We analyzed the distribution of voltage levels sufficient to cause electroporation in enzymatically isolated frog cardiac cells, using the cell-attached patch-clamp technique with rectangular pulses similar to those used in experimental studies of cardiac defibrillation. Five-millisecond monophasic or ten-millisecond biphasic symmetric (1/1) and asymmetric (1/0.5) rectangular pulses of either polarity were applied to the cell membrane in 100-mV steps from 0.2 to 0.8 V. The membrane conductance was continuously monitored by a low-voltage pulse train. In a total of 77 cells, we observed a step increase in conductance, occurring in 21% of cells at a transmembrane potential of 0.3 V, 52% at 0.4 V, 14% at 0.5 V, and 13% at 0.6-0.8 V. Electroporation occurred with this voltage distribution regardless of pulse shape, polarity, or the presence of all of the following ionic channel blockers: tetrodotoxin, barium, tetraethylammonium, 4-aminopyridine, cadmium, nickel, and gadolinium. The time course of membrane recovery was highly variable. The maintenance of a high membrane conductance after the shock pulse was associated with irreversible cell contracture provided that Ca2+ was included in the patch-pipette solution. However, with biphasic asymmetric pulses, the conductance recovered very quickly (< or = 37 ms).(ABSTRACT TRUNCATED AT 250 WORDS)

Nonlinear Changes of Transmembrane Potential During Electrical Shocks

“…This is significantly lower than the electroporation threshold of Ϸ300 mV reported from measurements of changes in membrane conductance in single frog myocytes in response to 5-ms-long voltage pulses. 25,26 The difference in thresholds between this and the present study could be attributable to differences in the pulse duration, different experimental conditions, as well as different cell species.…”

The influence of cell dimensions on the vulnerability of ventricular myocytes to lethal injury by high-intensity electrical fields

“…Differently from threshold excitation, which is a clear-cut phenomenon, electropermeabilization is graded with regard to both extension and pore lifetime, depending on shock parameters, such as intensity and duration (Fedorov et al, 2008;Neunlist and Tung, 1997;Oliveira et al, 2005;Tovar and Tung, 1992). Possibly for this reason, the range of the critical V m for permeabilization described for cardiac myocytes and millisecond shock duration is quite wide (250-1000 mV) (e.g., Cheek and Fast, 2004;Neunlist and Tung, 1997;O'Neill and Tung, 1991;Tovar and Tung, 1992).…”

“…Possibly for this reason, the range of the critical V m for permeabilization described for cardiac myocytes and millisecond shock duration is quite wide (250-1000 mV) (e.g., Cheek and Fast, 2004;Neunlist and Tung, 1997;O'Neill and Tung, 1991;Tovar and Tung, 1992). However, in the case of HIEF-induced cell death, it is plausible to conclude that permeabilization should be sufficiently extensive and long-lasting to allow sustained calcium overload and disruption of cell structure.…”

Irreversible Electroporation Ablation of Liver Metastases Adjacent to the Heart Induces Ventricular Tachycardia: A Case Report

“…As a result, some pulses were delivered during the vulnerable period of the ventricular myocardium, which corresponds to almost the entire T wave as seen on the ECG [12]. As rhythmic cardiac contraction is governed by the discharge of electrical impulses (action potentials) by the sinoatrial node [13], external electrical stimuli can lead to localized depolarization through the opening of non-specific ion channels [14][15][16]. Moreover, electrical stimuli that exceed the threshold excitation potential may cause localized depolarization to build into an action potential [17].…”