| Postconditioning inhibits mitochondrial permeability transition. | |
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MedLine Citation:
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PMID: 15642769 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Brief periods of ischemia performed just at the time of reperfusion can reduce infarct size, a phenomenon called "postconditioning." After reflow, opening of the mitochondrial permeability transition pore (mPTP) has been involved in lethal reperfusion injury. We hypothesized that postconditioning may modulate mPTP opening. METHODS AND RESULTS: Anesthetized open-chest rabbits underwent 30 minutes of ischemia and 4 hours of reperfusion. Control hearts underwent no additional intervention. Postconditioning consisted of 4 episodes of 1 minute of coronary occlusion and 1 minute of reperfusion performed after 1 minute of reflow after the prolonged ischemia. Preconditioning consisted of 5 minutes of ischemia and 5 minutes of reperfusion before the 30-minute ischemia. An additional group of rabbits received 5 mg/kg IV of NIM811, a specific inhibitor of the mPTP, 1 minute before reperfusion. Infarct size was assessed by triphenyltetrazolium staining. Mitochondria were isolated from the risk region myocardium, and Ca2+-induced mPTP opening was assessed by use of a potentiometric method. Postconditioning, preconditioning, and NIM811 significantly limited infarct size, which averaged 29+/-4%, 18+/-4%, and 20+/-4% of the risk region, respectively, versus 61+/-6% in controls (P< or =0.001 versus control). The Ca2+ load required to open the mPTP averaged 41+/-4, 47+/-5, and 67+/-9 micromol/L CaCl2 per mg of mitochondrial proteins in postconditioning, preconditioning, and NIM811, respectively, significantly higher than the value of 16+/-4 micromol/L per mg in controls (P< or =0.05). CONCLUSIONS: Postconditioning inhibits opening of the mPTP and provides a powerful antiischemic protection. |
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Authors:
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Laurent Argaud; Odile Gateau-Roesch; Olivier Raisky; Joseph Loufouat; Dominique Robert; Michel Ovize |
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Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't Date: 2005-01-10 |
Journal Detail:
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Title: Circulation Volume: 111 ISSN: 1524-4539 ISO Abbreviation: Circulation Publication Date: 2005 Jan |
Date Detail:
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Created Date: 2005-01-19 Completed Date: 2005-07-12 Revised Date: 2009-11-19 |
Medline Journal Info:
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Nlm Unique ID: 0147763 Medline TA: Circulation Country: United States |
Other Details:
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Languages: eng Pagination: 194-7 Citation Subset: AIM; IM |
Affiliation:
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INSERM E 0226, Université Claude Bernard Lyon I, France. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Apoptosis / drug effects, physiology Calcium / metabolism* Coronary Disease / physiopathology* Cyclosporine / therapeutic use* Extracellular Signal-Regulated MAP Kinases / physiology Ion Channel Gating / drug effects, physiology* Ion Channels / drug effects, physiology* Ion Transport / drug effects, physiology MAP Kinase Signaling System / drug effects, physiology Male Membrane Potentials Mitochondria, Heart / drug effects, physiology* Mitochondrial Membrane Transport Proteins Myocardial Infarction / etiology, pathology Myocardial Ischemia / complications, drug therapy, therapy* Myocardial Reperfusion Injury / enzymology, physiopathology, prevention & control* Necrosis Oxidative Stress Protein-Serine-Threonine Kinases / physiology Proto-Oncogene Proteins / physiology Proto-Oncogene Proteins c-akt Rabbits Random Allocation Time Factors |
| Chemical | |
Reg. No./Substance:
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0/Ion Channels; 0/Mitochondrial Membrane Transport Proteins; 0/Proto-Oncogene Proteins; 0/mitochondrial permeability transition pore; 143205-42-9/(melle-4)cyclosporin; 59865-13-3/Cyclosporine; 7440-70-2/Calcium; EC 2.7.11.1/Protein-Serine-Threonine Kinases; EC 2.7.11.1/Proto-Oncogene Proteins c-akt; EC 2.7.11.24/Extracellular Signal-Regulated MAP Kinases |
| Comments/Corrections | |
Comment In:
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Circulation. 2005 Jun 21;111(24):e442; author reply e442
[PMID:
15967857
]
Circulation. 2005 Jan 18;111(2):120-1 [PMID: 15657384 ] |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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