Document Detail


Exercise enhances myocardial ischemic tolerance via an opioid receptor-dependent mechanism.
MedLine Citation:
PMID:  17951371     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Eric W Dickson; Christopher P Hogrefe; Paula S Ludwig; Laynez W Ackermann; Lynn L Stoll; Gerene M Denning
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2007-10-19
Journal Detail:
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:
Created Date:  2008-01-14     Completed Date:  2008-02-28     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H402-8     Citation Subset:  IM    
Affiliation:
Department of Emergency Medicine, University of Iowa Hospitals and Clinics, 200 Hawkins Drive, Iowa City, IA 52242-1009, USA. eric-dickson@uiowa.edu
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MeSH Terms
Descriptor/Qualifier:
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:
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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