title: Anti-apoptotic effect of hyperbaric oxygen preconditioning on a rat model of myocardial infarction.
abstract: BACKGROUND
  In our previous study, it was indicated that hyperbaric oxygen preconditioning (HOP) could induce a preconditioning against myocardial infarction and promote neovascularization. In this study, attempts were made to investigate whether a modified short-term pre-exposure protocol could also induce cardioprotection, and its potential mechanisms.
  
  
  METHODS
  Adult male Sprague Dawley rats were divided into seven groups; group 1 was sham surgery (SHAM) and group 2 was pre-exposed to normal air (CTL), and the other groups to HOP 1, 6, 24, 48, and 72 h (H1, H6, H24, H48, H72 groups) before permanent ischemia. The infarct size was measured by triphenyltetrazolium chloride staining, and left ventricular function parameters were recorded. The extent of apoptosis was determined by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive staining. Caspase-3 activity, Bcl-2, and Bax expression were also measured.
  
  
  RESULTS
  Compared with CTL group, myocardial infarct size was significantly decreased as well as cardiac cell apoptosis in area at risk zones (AAR) in H48 group. Meanwhile, the activity of caspase 3 was reduced, the ratio of Bcl-2/Bax expression was up-regulated, and the heart function parameters, including left ventricular systolic pressure (LVSP), left ventricular diastolic pressure (LVEDP), +(dP/dt)(max), and -(dP/dt)(max) were also significantly improved after preconditioning in H48 group.
  
  
  CONCLUSIONS
  The results indicate that short-term HOP could induce cardioprotection and may not last for more than 24 h. HOP prevents myocardium from permanent ischemia injury by suppression of apoptotic pathways.
authors.affiliation: Department of Diving Medicine, Faculty of Naval Medicine, Second Military Medical University, Shanghai, PR China.
authors.forename: Qiang
authors.initials: Q
authors.lastname: Sun
authors.forename: Qing
authors.initials: Q
authors.lastname: Sun
authors.forename: Yun
authors.initials: Y
authors.lastname: Liu
authors.forename: Xuejun
authors.initials: X
authors.lastname: Sun
authors.forename: Hengyi
authors.initials: H
authors.lastname: Tao
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D053148:Caspase 3 / Q000378:metabolism; D004195:Disease Models, Animal; D006931:Hyperbaric Oxygenation / Q000379:methods*; D020287:In Situ Nick-End Labeling; D019157:Ischemic Preconditioning, Myocardial / Q000379:methods*; D008297:Male; D009203:Myocardial Infarction / Q000378:metabolism / Q000473:pathology* / Q000628:therapy*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D018919:Neovascularization, Physiologic / Q000502:physiology; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: C494828:Bax protein, rat; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; C505410:Casp3 protein, rat; D053148:Caspase 3