Document Detail


Late phase ischemic preconditioning preserves mitochondrial oxygen metabolism and attenuates post-ischemic myocardial tissue hyperoxygenation.
MedLine Citation:
PMID:  21050865     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
AIMS: Late phase ischemic preconditioning (LPC) protects the heart against ischemia-reperfusion (I/R) injury. However, its effect on myocardial tissue oxygenation and related mechanism(s) is unknown. The aim of the current study is to determine whether LPC attenuates post-ischemic myocardial tissue hyperoxygenation through preserving mitochondrial oxygen metabolism.
MAIN METHODS: C57BL/6 mice were subjected to 30 min coronary ligation followed by 60 min or 24 h reperfusion with or without LPC (3 cycles of 5 min I/5 min R): Sham, LPC, I/R, and LPC+I/R group. Myocardial tissue Po(2) and redox status were measured with electron paramagnetic resonance (EPR) spectroscopy.
KEY FINDINGS: Upon reperfusion, tissue Po(2) rose significantly above the pre-ischemic level in the I/R mice (23.1 ± 2.2 vs. 12.6 ± 1.3 mmHg, p<0.01). This hyperoxygenation was attenuated by LPC in the LPC+I/R mice (11.9 ± 2.0 mmHg, p<0.01). Activities of NADH dehydrogenase (NADH-DH), succinate-cytochrome c reductase (SCR) and cytochrome c oxidase (CcO) were preserved or increased in the LPC group, significantly reduced in the I/R group, and conserved in the LPC+I/R group. Manganese superoxide dismutase (Mn-SOD) protein expression was increased by LPC in the LPC and LPC+I/R mice compared to that in the Sham control (1.24 ± 0.01 and 1.23 ± 0.01, p<0.05). Tissue redox status was shifted to the oxidizing state with I/R (0.0268 ± 0.0016/min) and was corrected by LPC in the LPC+I/R mice (0.0379 ± 0.0023/min). Finally, LPC reduced the infarct size in the LPC+I/R mice (10.5 ± 0.4% vs. 33.3 ± 0.6%, p<0.05).
SIGNIFICANCE: Thus, LPC preserved mitochondrial oxygen metabolism, attenuated post-ischemic myocardial tissue hyperoxygenation, and reduced I/R injury.
Authors:
Yuanjing Li; Ming Cai; Yi Xu; Harold M Swartz; Guanglong He
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-11-02
Journal Detail:
Title:  Life sciences     Volume:  88     ISSN:  1879-0631     ISO Abbreviation:  Life Sci.     Publication Date:  2011 Jan 
Date Detail:
Created Date:  2010-12-27     Completed Date:  2011-01-21     Revised Date:  2013-07-03    
Medline Journal Info:
Nlm Unique ID:  0375521     Medline TA:  Life Sci     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  57-64     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 Elsevier Inc. All rights reserved.
Affiliation:
The Center for Biomedical EPR Spectroscopy and Imaging, Davis Heart and Lung Research Institute and Division of Cardiovascular Medicine, Department of Internal Medicine, The Ohio State University College of Medicine, Columbus, OH 43210, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Blotting, Western
Electron Spin Resonance Spectroscopy
Electron Transport Complex IV / metabolism
Ischemic Preconditioning, Myocardial*
Male
Mice
Mice, Inbred C57BL
Mitochondria, Heart / metabolism*,  physiology
Myocardial Infarction / enzymology,  metabolism,  physiopathology
Myocardial Reperfusion Injury / metabolism,  physiopathology,  prevention & control*
Myocardium / enzymology,  metabolism
NADH Dehydrogenase / metabolism
Oxidation-Reduction
Oxygen / metabolism
Regional Blood Flow / physiology
Succinate Cytochrome c Oxidoreductase / metabolism
Grant Support
ID/Acronym/Agency:
HL081630/HL/NHLBI NIH HHS; HL081630-04S1/HL/NHLBI NIH HHS; P01 EB002180/EB/NIBIB NIH HHS; P01EB2180/EB/NIBIB NIH HHS; R01 HL081630/HL/NHLBI NIH HHS; R01 HL081630-01/HL/NHLBI NIH HHS; R01 HL081630-02/HL/NHLBI NIH HHS; R01 HL081630-03/HL/NHLBI NIH HHS; R01 HL081630-04/HL/NHLBI NIH HHS; R01 HL081630-04S1/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
7782-44-7/Oxygen; EC 1.-/Succinate Cytochrome c Oxidoreductase; EC 1.6.99.3/NADH Dehydrogenase; EC 1.9.3.1/Electron Transport Complex IV
Comments/Corrections

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