Document Detail

Exercise induces early and late myocardial preconditioning in dogs.
MedLine Citation:
PMID:  12160953     Owner:  NLM     Status:  MEDLINE    
OBJECTIVE: We tested the hypothesis that exercise induces myocardial preconditioning in dogs. METHODS: We instrumented dogs with a snare on the anterior descending coronary artery and catheters in the root of the aorta, left ventricular cavity and coronary sinus. After recovering from surgery the dogs were trained to stay in the laboratory and run on a treadmill. Subsequently, they were randomly allocated to five groups: (1) non-preconditioned dogs: under anesthesia, the anterior descending coronary artery was occluded during 1 h and then reperfused during 4.5 h. (2) Early preconditioned dogs: procedure similar to group 1 but the dogs performed exercise on a treadmill for five periods of 5 min each before the coronary occlusion. (3) Late preconditioned dogs: procedure similar to group 2 but 24 h were allowed to elapse between the preconditioning exercise and the coronary occlusion. (4) Early preconditioned dogs plus 5-hydroxydecanoate: procedure similar to group 2 but 5-hydroxydecanoate was administered prior to exercise. (5) Non-preconditioned dogs with 5-hydroxydecanoate: procedure similar to group 1 but 5-hydroxydecanoate was administered at a time equivalent to that in group 4. RESULTS: Exercise did not induce myocardial ischemia and the hemodynamics during the experiments did not differ between groups. Exercise immediately before the coronary occlusion decreased the infarct size (percent of the risk region) by 78% (P<0.05), an effect that was abolished with 5-hydroxydecanoate. Exercise 24 h prior to coronary occlusion decreased infarct size by 46% (P<0.05 vs. non-preconditioned dogs, P<0.05 vs. early preconditioned dogs). 5-Hydroxydecanoate by itself did not modify infarct size. These effects could not be explained by changes in collateral flow to the ischemic region. CONCLUSIONS: Exercise prior to a coronary occlusion induces early and late preconditioning of the infarct size. The early effect is mediated through mitochondrial ATP-sensitive potassium channels.
Raúl Domenech; Pilar Macho; Hermann Schwarze; Gina Sánchez
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Cardiovascular research     Volume:  55     ISSN:  0008-6363     ISO Abbreviation:  Cardiovasc. Res.     Publication Date:  2002 Aug 
Date Detail:
Created Date:  2002-08-05     Completed Date:  2002-11-05     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0077427     Medline TA:  Cardiovasc Res     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  561-6     Citation Subset:  IM    
Department of Pathophysiology, Biomedical Sciences Institute, Faculty of Medicine, University of Chile, Casilla 16038, Santiago 9, Chile.
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MeSH Terms
Analysis of Variance
Decanoic Acids / pharmacology
Hydroxy Acids / pharmacology
Ischemic Preconditioning, Myocardial / methods*
Mitochondria, Heart / drug effects,  metabolism
Models, Animal
Myocardial Infarction / metabolism,  prevention & control*
Physical Conditioning, Animal*
Potassium Channel Blockers / pharmacology
Potassium Channels / metabolism
Random Allocation
Time Factors
Reg. No./Substance:
0/Decanoic Acids; 0/Hydroxy Acids; 0/Potassium Channel Blockers; 0/Potassium Channels; 624-00-0/5-hydroxydecanoic acid

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