title: Effect of prolonged hypothermic ischemia and reperfusion on oxygen consumption and total mechanical energy in rat myocardium: participation of mitochondrial oxidative phosphorylation.
abstract: BACKGROUND
  To reduce ischemia-reperfusion injury of hearts in open heart surgery and transplantation, it is important to know the critical period of ischemia in which donor hearts can sustain their function satisfactorily. Cardiac function has been deduced from oxygen consumption (VO2) and mechanical parameters such as pressure-volume area (PVA). Inhibited mitochondrial oxidative phosphorylation during ischemia indicates that ATP production is uncoupled from VO2. Therefore, both mitochondrial oxidative phosphorylation and total mechanical energy should be examined to evaluate cardiac function after ischemia and reperfusion.
  
  
  METHODS
  Isolated rat hearts were stored in Euro-Collins solution at 4 degrees C for 8, 12, and 24 hr and reperfused in a working mode with a modified Krebs-Henseleit bicarbonate solution. PVA and VO2 were examined in isovolumic contraction, and ventricular contractility and total mechanical energy were assessed, respectively, by the end-systolic elastance (Ees) and PVA. Mitochondrial oxidative phosphorylation in the presence of succinate and mitochondrial lipid peroxide levels were estimated in similarly treated rat hearts.
  
  
  RESULTS
  Ees was decreased by ischemia without significant difference. The VO2 to PVA ratio remained linear, although VO2 at null PVA and the VO2 to PVA ratio significantly increased after 12 hr of ischemia. Mitochondrial oxidative phosphorylation was decreased significantly by reperfusion after 12 hr of ischemia. Mitochondrial lipid peroxide levels were increased significantly after 12 hr of ischemia.
  
  
  CONCLUSIONS
  In isolated rat hearts, decreased efficiency for energy conversion from consumed oxygen to cardiac performance occurs between 8 and 12 hr of hypothermic ischemia, which was coincident with disturbed mitochondrial oxidative phosphorylation, to which lipid peroxidation may contribute.
authors.affiliation: Second Department of Surgery, Miyazaki Medical College, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Kuwabara
authors.forename: H
authors.initials: H
authors.lastname: Takenaka
authors.forename: H
authors.initials: H
authors.lastname: Maruyama
authors.forename: T
authors.initials: T
authors.lastname: Onitsuka
authors.forename: M
authors.initials: M
authors.lastname: Hamada
mesh_terms: D000818:Animals; D006321:Heart / Q000502:physiology; D007035:Hypothermia / Q000378:metabolism; D015227:Lipid Peroxidation; D008297:Male; D008929:Mitochondria, Heart / Q000378:metabolism; D009200:Myocardial Contraction; D015428:Myocardial Reperfusion Injury / Q000378:metabolism* / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism; D010085:Oxidative Phosphorylation; D010101:Oxygen Consumption / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000378:metabolism* / Q000503:physiopathology*; D018924:Vascular Capacitance