| Exercise enhances myocardial ischemic tolerance via an opioid receptor-dependent mechanism. | |
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MedLine Citation:
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PMID: 17951371 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Exercise increases serum opioid levels and improves cardiovascular health. Here we tested the hypothesis that opioids contribute to the acute cardioprotective effects of exercise using a rat model of exercise-induced cardioprotection. For the standard protocol, rats were randomized to 4 days of treadmill training and 1 day of vigorous exercise (day 5), or to a sham exercise control group. On day 6, animals were killed, and global myocardial ischemic tolerance was assessed on a modified Langendorff apparatus. Twenty minutes of ischemia followed by 3 h of reperfusion resulted in a mean infarct size of 42 +/- 4% in hearts from sham exercise controls and 21 +/- 3% (P < 0.001) in the exercised group. The cardioprotective effects of exercise were gone by 5 days after the final exercise period. To determine the role of opioid receptors in exercise-induced cardioprotection, rats were exercised according to the standard protocol; however, just before exercise on days 4 and 5, rats were injected subcutaneously with 10 mg/kg of the opioid receptor antagonist naltrexone. Similar injections were performed in the sham exercise control group. Naltrexone had no significant effect on baseline myocardial ischemic tolerance in controls (infarct size 43 +/- 4%). In contrast, naltrexone treatment completely blocked the cardioprotective effect of exercise (infarct size 40 +/- 5%). Exercise was also associated with an early increase in myocardial mRNA levels for several opioid system genes and with sustained changes in a number of genes that regulate inflammation and apoptosis. These findings demonstrate that the acute cardioprotective effects of exercise are mediated, at least in part, through opioid receptor-dependent mechanisms that may include changes in gene expression. |
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Authors:
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Eric W Dickson; Christopher P Hogrefe; Paula S Ludwig; Laynez W Ackermann; Lynn L Stoll; Gerene M Denning |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2007-10-19 |
Journal Detail:
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Title: American journal of physiology. Heart and circulatory physiology Volume: 294 ISSN: 0363-6135 ISO Abbreviation: Am. J. Physiol. Heart Circ. Physiol. Publication Date: 2008 Jan |
Date Detail:
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Created Date: 2008-01-14 Completed Date: 2008-02-28 Revised Date: 2008-11-21 |
Medline Journal Info:
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Nlm Unique ID: 100901228 Medline TA: Am J Physiol Heart Circ Physiol Country: United States |
Other Details:
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Languages: eng Pagination: H402-8 Citation Subset: IM |
Affiliation:
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Department of Emergency Medicine, University of Iowa Hospitals and Clinics, 200 Hawkins Drive, Iowa City, IA 52242-1009, USA. eric-dickson@uiowa.edu |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Apoptosis / genetics Disease Models, Animal Gene Expression Inflammation / genetics, metabolism Male Myocardial Ischemia / complications, genetics, metabolism, pathology, prevention & control* Myocardial Reperfusion Injury / etiology, genetics, metabolism, pathology, prevention & control* Myocardium / metabolism*, pathology Naltrexone / pharmacology Narcotic Antagonists / pharmacology Opioid Peptides / genetics, metabolism* Physical Exertion* Protein Precursors / genetics, metabolism* RNA, Messenger / metabolism Rats Rats, Sprague-Dawley Receptors, Opioid / antagonists & inhibitors, genetics, metabolism* Time Factors |
| Chemical | |
Reg. No./Substance:
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0/Narcotic Antagonists; 0/Opioid Peptides; 0/Protein Precursors; 0/RNA, Messenger; 0/Receptors, Opioid; 16590-41-3/Naltrexone |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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