title: Accelerated glycolysis and greater postischemic dysfunction in hypertrophied rat hearts are independent of coronary flow.
abstract: BACKGROUND
  After ischemia, glycolysis and dysfunction are greater, while coupling of glucose oxidation to glycolysis is lower in hypertrophied hearts than in nonhypertrophied hearts.
  
  
  OBJECTIVE
  To test the hypothesis that accelerated glycolysis, reduced coupling of glucose oxidation to glycolysis and increased postischemic dysfunction in hypertrophied hearts compared with nonhypertrophied hearts occur in the absence of differences in coronary flow.
  
  
  METHODS
  Function, glycolysis and glucose oxidation were measured in isolated working control and hypertrophied rat hearts studied for 30 min before, and for 40 min after no flow global ischemia for 20 min under conditions in which coronary flow was comparable between the two groups. The hearts were perfused with 1.2 mmol/L palmitate, 5.5 mmol/L [5-3H/U-14C]-glucose, 0.5 mmol/L lactate, 100 mU/L insulin at a preload of 11.5 mmHg, and an afterload of 60 mmHg in control hearts or 80 mmHg in hypertrophied hearts.
  
  
  RESULTS
  Despite comparable rates of coronary flow, functional recovery was lower in hypertrophied hearts than in control hearts. The rates of glycolysis were accelerated in hypertrophied hearts, while glucose oxidation did not significantly differ between the two groups. As a result, the coupling of glucose oxidation to glycolysis was lower in hypertrophied hearts than in control hearts.
  
  
  CONCLUSIONS
  Increased postischemic dysfunction, accelerated glycolysis and reduced coupling of glucose oxidation to glycolysis in hypertrophied hearts compared with control hearts cannot be accounted for by differences in coronary flow. These data provide support for the concept that alterations in glucose metabolism contribute to the exaggerated postischemic dysfunction of hypertrophied hearts.
authors.affiliation: McDonald Research Laboratories/iCapture Center, Department of Pathology and Laboratory Medicine, University of British Columbia, St Paul's Hospital, 1081 Burrard Street, Vancouver, British Columbia V6Z 1Y6, Canada.
authors.forename: R B
authors.initials: RB
authors.lastname: Wambolt
authors.forename: M
authors.initials: M
authors.lastname: Grist
authors.forename: G P
authors.initials: GP
authors.lastname: Bondy
authors.forename: M F
authors.initials: MF
authors.lastname: Allard
mesh_terms: D000818:Animals; D003326:Coronary Circulation / Q000502:physiology*; D004195:Disease Models, Animal; D005947:Glucose / Q000378:metabolism*; D006019:Glycolysis / Q000502:physiology*; D017379:Hypertrophy, Left Ventricular / Q000503:physiopathology* / Q000628:therapy; D008297:Male; D017202:Myocardial Ischemia / Q000503:physiopathology*; D011336:Probability; D051381:Rats; D017207:Rats, Sprague-Dawley; D020127:Recovery of Function; D012016:Reference Values; D015427:Reperfusion Injury / Q000473:pathology*
chemical_list: D005947:Glucose