| Preservation of mitochondrial function with cardiopulmonary resuscitation in prolonged cardiac arrest in rats. | |
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MedLine Citation:
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PMID: 19751739 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Steve T Yeh; Hsin-Ling Lee; Sverre E Aune; Chwen-Lih Chen; Yeong-Renn Chen; Mark G Angelos |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2009-09-12 |
Journal Detail:
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Title: Journal of molecular and cellular cardiology Volume: 47 ISSN: 1095-8584 ISO Abbreviation: J. Mol. Cell. Cardiol. Publication Date: 2009 Dec |
Date Detail:
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Created Date: 2009-11-09 Completed Date: 2010-03-08 Revised Date: 2011-03-03 |
Medline Journal Info:
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Nlm Unique ID: 0262322 Medline TA: J Mol Cell Cardiol Country: England |
Other Details:
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Languages: eng Pagination: 789-97 Citation Subset: IM |
Affiliation:
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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:
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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:
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HL083237/HL/NHLBI NIH HHS; R01 HL083237-02/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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9035-34-1/Cytochromes a |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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