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Spatial Distribution and Extent of Electroporation by Strong Internal Shock in Intact Structurally Normal and Chronically Infarcted Rabbit Hearts


  • This study was supported by the National Institutes of Health (Dr. Efimov; R01 HL074283) and the American Heart Association (Dr. Cheng; 0235172N and 0655154B).

  • Manuscript received 4 January 2008; Revised manuscript received 11 March 2008; Accepted for publication 14 March 2008.

Address for correspondence: Yuanna Cheng, M.D., Ph.D., Department of Molecular Cardiology, NE61, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195, USA. Fax: 216-445-4166; E-mail:


Introduction: Although life-saving, a strong internal defibrillation shock may temporarily or permanently damage the heart via disruption of cell membranes (electroporation). Spatial extent of electroporation in intact, normal, or infarcted hearts has not been investigated. In this study, shock-induced electroporation in intact rabbit hearts with and without chronic (>4 weeks) left ventricular myocardial infarction (MI) was characterized. 

Methods and Results: A coil shock electrode was inserted in the right ventricle of Langendorff-perfused hearts. One truncated exponential monophasic shock (+300 V, 8 ms) was delivered by a 150 μF capacitor clinical defibrillator while the heart was perfused with membrane-impermeant dye propidium iodide (PI). The heart was sectioned transversely, and uptake of PI into ventricular myocardium through electropores was quantified. Histological evaluation was performed via Masson's trichrome staining. PI accumulation was minimal in the control (n = 3) and MI (n = 3) hearts without shock. Following shock delivery, (1) in control (n = 5) and MI (n = 5) hearts, electroporation mostly occurred near the shock electrode and was longitudinally distributed along the active region of the shock electrode; (2) in MI group, electroporation was significantly increased (P < 0.05) in the surviving anterior epicardial layers of the infarcted region; and (3) between the control and MI groups, the overall extent of electroporation was similar. 

Conclusion: Shock-induced electroporation was spatially dependent on the location and dimension of the active region of the shock electrode. The overall extent of electroporation in the MI heart was comparable with the control heart, but the surviving anterior epicardial layers in the infarcted region were more susceptible to electroporation.