title: Hypoxic preconditioning preserves antioxidant reserve in the working rat heart.
abstract: OBJECTIVE
  The aim was to examine whether intracellular antioxidants play a role in myocardial preservation following hypoxic preconditioning.
  
  
  METHODS
  Isolated working rat hearts were subjected to 30 min ischaemia and 30 min reperfusion. Control hearts were compared to hearts preconditioned with 10 min hypoxia. Left ventricular function and lactate dehydrogenase (LDH) release were measured in each group. Ascorbate dependent (ADAR) and thiol dependent (TDAR) components of the endogenous myocardial antioxidant reserve were assessed using electron spin resonance spectroscopy.
  
  
  RESULTS
  a Hypoxic preconditioning had no effect on left ventricular function after 10 min reoxygenation. During reperfusion, the hypoxically preconditioned hearts had a significantly increased survival rate, aortic flow, developed pressure, and dP/dtmax, and a reduced lactate dehydrogenase release, compared to non-preconditioned controls (P < 0.05). Preconditioned hearts also had significantly higher preservation of baseline ADAR (79%) and TDAR (96%) compared with control hearts, (70%) and (77%), respectively (P < 0.05).
  
  
  CONCLUSIONS
  Hypoxic preconditioning enhances functional recovery and reduces cell necrosis following global ischaemia in the working rat heart. This phenomenon may, in part, be mediated through enhanced ascorbate and thiol components of the antioxidant reserve.
authors.affiliation: Department of Surgery, University of Connecticut School of Medicine, Farmington 06030-1110.
authors.forename: D T
authors.initials: DT
authors.lastname: Engelman
authors.forename: M
authors.initials: M
authors.lastname: Watanabe
authors.forename: R M
authors.initials: RM
authors.lastname: Engelman
authors.forename: J A
authors.initials: JA
authors.lastname: Rousou
authors.forename: E
authors.initials: E
authors.lastname: Kisin
authors.forename: V E
authors.initials: VE
authors.lastname: Kagan
authors.forename: N
authors.initials: N
authors.lastname: Maulik
authors.forename: D K
authors.initials: DK
authors.lastname: Das
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D001205:Ascorbic Acid / Q000378:metabolism; D004578:Electron Spin Resonance Spectroscopy; D006321:Heart / Q000503:physiopathology; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008297:Male; D009203:Myocardial Infarction / Q000517:prevention & control*; D017202:Myocardial Ischemia / Q000378:metabolism* / Q000503:physiopathology; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000378:metabolism*; D010477:Perfusion; D051381:Rats; D017207:Rats, Sprague-Dawley; D013438:Sulfhydryl Compounds / Q000378:metabolism; D013997:Time Factors
chemical_list: D000975:Antioxidants; D013438:Sulfhydryl Compounds; D007770:L-Lactate Dehydrogenase; D001205:Ascorbic Acid