Document Detail


Direct current shocks to the heart generate free radicals: an electron paramagnetic resonance study.
MedLine Citation:
PMID:  8917277     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVES: We sought to demonstrate that direct current (DC) shocks to the heart generate free radicals. BACKGROUND: Although it is a lifesaving maneuver, defibrillation is known to have myocardial toxicity. The mechanism of this toxicity is unknown. If DC shocks generate free radicals, free radicals could be a mechanism of myocardial injury. METHODS: In a canine model, DC shocks of 10 to 100 J were delivered to the epicardium of both beating and fibrillating hearts, and 200-J transthoracic shocks were administered in dogs with beating hearts. Ascorbate free radical (AFR) concentration was measured in arterial blood and blood continuously withdrawn from the coronary sinus. In some dogs, the antioxidant enzymes superoxide dismutase (15,000 U/kg) and catalase (55,000 U/kg) (SOD/Cat) were administered before shocks. RESULTS: Ascorbate free radicals were generated by DC shocks. A peak AFR increase of 14 +/- 2% (mean +/- SEM) was seen 5 to 6 min after 100-J epicardial shocks. A peak AFR increase of 7 +/- 5% occurred after transthoracic shocks. There was a significant linear relation between the shock energy and peak percent AFR increase: %AFR increase = 0.18 (Shock energy) + 2.9 (r = 0.73, p < 0.0001). Shocks delivered to hearts in ventricular fibrillation (30 s) resulted in generation of AFR equal to but not greater than that observed during similar shocks delivered to beating hearts in sinus rhythm. Multiple successive shocks (100 J delivered twice or five times) did not result in a greater AFR increase than single 100-J shocks, indicating that peak, not cumulative, energy is the principal determinant of AFR increase. Animals receiving SOD/Cat before shock administration showed significant attenuation of the AFR increase. CONCLUSIONS: Direct current epicardial and transthoracic shocks generate free radicals; antioxidant enzymes reduce the free radical generation by shocks.
Authors:
M R Caterine; K T Spencer; L A Pagan-Carlo; R S Smith; G R Buettner; R E Kerber
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Journal of the American College of Cardiology     Volume:  28     ISSN:  0735-1097     ISO Abbreviation:  J. Am. Coll. Cardiol.     Publication Date:  1996 Nov 
Date Detail:
Created Date:  1996-12-11     Completed Date:  1996-12-11     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  8301365     Medline TA:  J Am Coll Cardiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1598-609     Citation Subset:  AIM; IM    
Affiliation:
Cardiovascular Center, University of Iowa, Iowa City 52242, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Catalase / administration & dosage,  metabolism
Dogs
Electric Countershock* / methods
Electron Spin Resonance Spectroscopy
Free Radicals / blood*
Myocardium / metabolism*
Superoxide Dismutase / administration & dosage,  metabolism
Ventricular Fibrillation / metabolism*,  therapy
Grant Support
ID/Acronym/Agency:
HL07121/HL/NHLBI NIH HHS; HL43098/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Free Radicals; EC 1.11.1.6/Catalase; EC 1.15.1.1/Superoxide Dismutase

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