title: Exercise induces early and late myocardial preconditioning in dogs.
abstract: 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.
authors.affiliation: Department of Pathophysiology, Biomedical Sciences Institute, Faculty of Medicine, University of Chile, Casilla 16038, Santiago 9, Chile. rdomenec@machi.med.uchile.cl
authors.forename: Raúl
authors.initials: R
authors.lastname: Domenech
authors.forename: Pilar
authors.initials: P
authors.lastname: Macho
authors.forename: Hermann
authors.initials: H
authors.lastname: Schwarze
authors.forename: Gina
authors.initials: G
authors.lastname: Sánchez
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D003652:Decanoic Acids / Q000494:pharmacology; D004285:Dogs; D006880:Hydroxy Acids / Q000494:pharmacology; D019157:Ischemic Preconditioning, Myocardial / Q000379:methods*; D008929:Mitochondria, Heart / Q000187:drug effects / Q000378:metabolism; D023421:Models, Animal; D009203:Myocardial Infarction / Q000378:metabolism / Q000517:prevention & control*; D010805:Physical Conditioning, Animal; D026902:Potassium Channel Blockers / Q000494:pharmacology; D015221:Potassium Channels / Q000378:metabolism; D011897:Random Allocation; D013997:Time Factors
chemical_list: D003652:Decanoic Acids; D006880:Hydroxy Acids; D026902:Potassium Channel Blockers; D015221:Potassium Channels; C052853:5-hydroxydecanoic acid