title: Preconditioning preserves mitochondrial function and glycolytic flux during an early period of reperfusion in perfused rat hearts.
abstract: OBJECTIVE
  The purpose of the present study was to examine the effects of preconditioning on glycolysis and oxidative phosphorylation during reperfusion in perfused rat hearts.
  
  
  METHODS
  Preconditioning was induced by 5 min of ischemia and 5 min of reperfusion before 40 min of sustained ischemia and subsequent 30 min of reperfusion. Tissue energy metabolite levels, mitochondrial oxygen consumption capacity and adenine nucleotide translocator content of the perfused hearts were assessed at 40 min of ischemia, 5 and 30 min of reperfusion.
  
  
  RESULTS
  Preconditioning improved the postischemic recovery of rate x pressure product (92.5 +/- 8.7 vs. 24.9 +/- 1.2% for non-preconditioned group) and high-energy phosphate content (ATP and CrP; 39.5 +/- 2.0 and 96.2 +/- 4.9% of initial vs. 24.1 +/- 0.9 and 56.1 +/- 4.3% of initial for the non-preconditioned group). The mitochondrial oxygen consumption capacity and the adenine nucleotide translocator content of the non-preconditioned heart were decreased by sustained ischemia and remained decreased throughout reperfusion. Preconditioning prevented these decreases. The tissue lactate level of the non-preconditioned heart was high throughout reperfusion (16.5-fold vs. basal), whereas in the preconditioned heart it returned to the basal level within a few minutes of reperfusion. Furthermore, the ratios of [fructose 1,6-bisphosphate]/([glucose 6-phosphate] + [fructose 6-phosphate]) at 5-min reperfusion were higher (2.2-fold) than those of the non-preconditioned heart.
  
  
  CONCLUSIONS
  The results suggest that preconditioning preserves the capacity for normal mitochondrial function and the facilitation of glycolysis during reperfusion, which may play an important role in the improvement of postischemic contractile function and high-energy phosphate content.
authors.affiliation: Department of Pharmacology, Tokyo University of Pharmacy and Life Science, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Yabe
authors.forename: Y
authors.initials: Y
authors.lastname: Nasa
authors.forename: M
authors.initials: M
authors.lastname: Sato
authors.forename: R
authors.initials: R
authors.lastname: Iijima
authors.forename: S
authors.initials: S
authors.lastname: Takeo
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D003576:Electron Transport Complex IV / Q000378:metabolism; D005636:Fructosephosphates / Q000378:metabolism; D005958:Glucosephosphates / Q000378:metabolism; D006019:Glycolysis; D019157:Ischemic Preconditioning, Myocardial; D008297:Male; D008929:Mitochondria, Heart / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D000226:Mitochondrial ADP, ATP Translocases / Q000378:metabolism; D017202:Myocardial Ischemia / Q000378:metabolism*; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000378:metabolism*; D010101:Oxygen Consumption; D051381:Rats; D017207:Rats, Sprague-Dawley; D012503:Saponins / Q000494:pharmacology
chemical_list: D005636:Fructosephosphates; D005958:Glucosephosphates; D012503:Saponins; D000255:Adenosine Triphosphate; D000226:Mitochondrial ADP, ATP Translocases; D003576:Electron Transport Complex IV