Document Detail


Preservation of mitochondrial function with cardiopulmonary resuscitation in prolonged cardiac arrest in rats.
MedLine Citation:
PMID:  19751739     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
During cardiac arrest (CA), myocardial perfusion is solely dependent on cardiopulmonary resuscitation (CPR) although closed-chest compressions only provide about 10-20% of normal myocardial perfusion. The study was conducted in a whole animal CPR model to determine whether CPR-generated oxygen delivery preserves or worsens mitochondrial function. Male Sprague-Dawley rats (400-450 g) were randomly divided into four groups: (1) BL (instrumentation only, no cardiac arrest), (2) CA(15) (15 min cardiac arrest without CPR), (3) CA(25) (25 min cardiac arrest without CPR) and (4) CPR (15 min cardiac arrest, followed by 10 min CPR). The differences between groups were evaluated by measuring mitochondrial respiration, electron transport chain (ETC) complex activities and mitochondrial ultrastructure by transmission electron microscopy (TEM). The CA(25) group had the greatest impairment of mitochondrial respiration and ETC complex activities (I-III). In contrast, the CPR group was not different from the CA(15) group regarding all measures of mitochondrial function. Complex I was more susceptible to ischemic injury than the other complexes and was the major determinant of mitochondrial dysfunction. Observations of mitochondrial ultrastructure by TEM were compatible with the biochemical results. The findings suggest that, despite low blood flow and oxygen delivery, CPR is able to preserve heart mitochondrial function and viability during ongoing global ischemia. Preservation of complex I activity and mitochondrial function during cardiac arrest may be an important mechanism underlying the beneficial effects of CPR which have been shown in clinical studies.
Authors:
Steve T Yeh; Hsin-Ling Lee; Sverre E Aune; Chwen-Lih Chen; Yeong-Renn Chen; Mark G Angelos
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2009-09-12
Journal Detail:
Title:  Journal of molecular and cellular cardiology     Volume:  47     ISSN:  1095-8584     ISO Abbreviation:  J. Mol. Cell. Cardiol.     Publication Date:  2009 Dec 
Date Detail:
Created Date:  2009-11-09     Completed Date:  2010-03-08     Revised Date:  2013-07-02    
Medline Journal Info:
Nlm Unique ID:  0262322     Medline TA:  J Mol Cell Cardiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  789-97     Citation Subset:  IM    
Affiliation:
Davis Heart and Lung Research Institute, The Ohio State University, Columbus, OH 43210, USA; Department of Emergency Medicine, The Ohio State University, Columbus, OH 43210, USA; Biophysics Graduate Program, The Ohio State University, Columbus, OH 43210, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Blotting, Western
Cardiopulmonary Resuscitation*
Cell Respiration
Cytochromes a / metabolism
Densitometry
Electron Transport
Heart Arrest / pathology,  physiopathology*
Male
Mitochondria, Heart / metabolism*,  ultrastructure
Rats
Rats, Sprague-Dawley
Grant Support
ID/Acronym/Agency:
HL083237/HL/NHLBI NIH HHS; R01 HL083237/HL/NHLBI NIH HHS; R01 HL083237-02/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
9035-34-1/Cytochromes a
Comments/Corrections

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


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