Document Detail

Electroporation induced by internal defibrillation shock with and without recovery in intact rabbit hearts.
MedLine Citation:
PMID:  22730387     Owner:  NLM     Status:  MEDLINE    
Defibrillation shocks from implantable cardioverter defibrillators can be lifesaving but can also damage cardiac tissues via electroporation. This study characterizes the spatial distribution and extent of defibrillation shock-induced electroporation with and without a 45-min postshock period for cell membranes to recover. Langendorff-perfused rabbit hearts (n = 31) with and without a chronic left ventricular (LV) myocardial infarction (MI) were studied. Mean defibrillation threshold (DFT) was determined to be 161.4 ± 17.1 V and 1.65 ± 0.44 J in MI hearts for internally delivered 8-ms monophasic truncated exponential (MTE) shocks during sustained ventricular fibrillation (>20 s, SVF). A single 300-V MTE shock (twice determined DFT voltage) was used to terminate SVF. Shock-induced electroporation was assessed by propidium iodide (PI) uptake. Ventricular PI staining was quantified by fluorescent imaging. Histological analysis was performed using Masson's Trichrome staining. Results showed PI staining concentrated near the shock electrode in all hearts. Without recovery, PI staining was similar between normal and MI groups around the shock electrode and over the whole ventricles. However, MI hearts had greater total PI uptake in anterior (P < 0.01) and posterior (P < 0.01) LV epicardial regions. Postrecovery, PI staining was reduced substantially, but residual staining remained significant with similar spacial distributions. PI staining under SVF was similar to previously studied paced hearts. In conclusion, electroporation was spatially correlated with the active region of the shock electrode. Additional electroporation occurred in the LV epicardium of MI hearts, in the infarct border zone. Recovery of membrane integrity postelectroporation is likely a prolonged process. Short periods of SVF did not affect electroporation injury.
Yves T Wang; Igor R Efimov; Yuanna Cheng
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2012-06-22
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  303     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2012 Aug 
Date Detail:
Created Date:  2012-08-16     Completed Date:  2012-10-26     Revised Date:  2013-08-18    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H439-49     Citation Subset:  IM    
Department of Molecular Cardiology, Cleveland Clinic, Cleveland, Ohio, USA.
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MeSH Terms
Cardiac Pacing, Artificial
Cell Membrane / pathology
Cell Membrane Permeability
Defibrillators, Implantable / adverse effects*
Disease Models, Animal
Electric Countershock / adverse effects*,  instrumentation
Heart Injuries / etiology*,  pathology,  physiopathology
Heart Ventricles / injuries,  pathology
Myocardial Infarction / complications*,  pathology,  physiopathology
Myocytes, Cardiac / pathology*
Recovery of Function
Time Factors
Ventricular Fibrillation / etiology,  pathology,  physiopathology,  therapy*
Grant Support

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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