Document Detail

Susceptibility of the heart to ischaemia-reperfusion injury and exercise-induced cardioprotection are sex-dependent in the rat.
MedLine Citation:
PMID:  15718263     Owner:  NLM     Status:  MEDLINE    
The cardioprotective effects of short-term exercise against myocardial ischaemia-reperfusion injury in male and female rats were examined. We subjected male and female rats to 0 (Sed; n = 8 males and 8 females), 1 (1 day; n = 10 males and 8 females), or 5 (5 day; n = 6 males and 6 females) days of treadmill running. Langendorff-perfused hearts underwent 1 h of regional ischaemia and 2 h of reperfusion, and infarct size (expressed as a percentage of the zone at risk; ZAR), left ventricular pressure development, and coronary flow were measured for each heart. Preischaemic pressure development and coronary flow did not differ between the sexes nor were they influenced by exercise. Sed females had significantly smaller infarct sizes (25 +/- 3%) than Sed male hearts (37 +/- 3%; P < 0.001). Short-term running significantly reduced infarct size following 1 day (27 +/- 3%; P < 0.05) and 5 days (30 +/- 4%; P < 0.10) of exercise in males. One day of running did not reduce infarct size in females (19 +/- 3%; P = NS), but 5 day females did show a significant reduction in infarct size (13 +/- 2%; P < 0.05). There was no relationship between postischaemic coronary vascular hyperaemia and infarct size across sexes or exercise training groups. Hearts from Sed females exhibited significantly higher manganese superoxide dismutase (MnSOD) protein expression than hearts from Sed males, but short-term exercise (neither 1 nor 5 days) did not alter MnSOD protein in either sex. Increased sarcolemmal ATP-sensitive K(+) (K(ATP)) channel subunit protein expression (SUR2A and/or K(ir)6.2) correlated closely with sex-dependent and exercise-acquired protection against myocardial infarction. These data indicate that: (1) sex-dependent and exercise-induced differences in the susceptibility of the heart to ischaemia-reperfusion injury are not associated with improved coronary flow or postischaemic hyperaemia; (2) increased MnSOD protein expression is not necessary for exercise-induced protection from infarction; and (3) one possible mechanism for sex-dependent and exercise-mediated reductions in infarct size involves an increased protein expression of cardiac sarcolemmal K(ATP) channels.
David A Brown; Joshua M Lynch; Casey J Armstrong; Nicholas M Caruso; Lindsay B Ehlers; Micah S Johnson; Russell L Moore
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.     Date:  2005-02-17
Journal Detail:
Title:  The Journal of physiology     Volume:  564     ISSN:  0022-3751     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2005 Apr 
Date Detail:
Created Date:  2005-04-13     Completed Date:  2005-08-23     Revised Date:  2010-09-20    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  619-30     Citation Subset:  IM    
Department of Integrative Physiology, University of Colorado Cardiovascular Institute, University of Colorado at Boulder, Boulder, CO 80309-0354, USA.
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MeSH Terms
Disease Susceptibility / physiopathology
Myocardial Reperfusion Injury / genetics,  metabolism*,  prevention & control*
Physical Conditioning, Animal / methods,  physiology*
Potassium Channels, Inwardly Rectifying / biosynthesis,  genetics
Rats, Sprague-Dawley
Sex Characteristics*
Superoxide Dismutase / biosynthesis,  genetics
Grant Support
Reg. No./Substance:
0/Kir6.2 channel; 0/Potassium Channels, Inwardly Rectifying; EC Dismutase

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