PMID- 20421116
OWN - NLM
STAT- MEDLINE
DCOM- 20120109
LR  - 20111017
IS  - 1095-8673 (Electronic)
IS  - 0022-4804 (Linking)
VI  - 171
IP  - 1
DP  - 2011 Nov
TI  - Anti-apoptotic effect of hyperbaric oxygen preconditioning on a rat model of 
      myocardial infarction.
PG  - 41-6
LID - 10.1016/j.jss.2010.01.036 [doi]
AB  - 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. MATERIALS AND 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. CONCLUSION: 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.
CI  - Copyright (c) 2011 Elsevier Inc. All rights reserved.
FAU - Sun, Qiang
AU  - Sun Q
AD  - Department of Diving Medicine, Faculty of Naval Medicine, Second Military Medical 
      University, Shanghai, PR China.
FAU - Sun, Qing
AU  - Sun Q
FAU - Liu, Yun
AU  - Liu Y
FAU - Sun, Xuejun
AU  - Sun X
FAU - Tao, Hengyi
AU  - Tao H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20100216
PL  - United States
TA  - J Surg Res
JT  - The Journal of surgical research
JID - 0376340
RN  - 0 (Bax protein, rat)
RN  - 0 (Proto-Oncogene Proteins c-bcl-2)
RN  - 0 (bcl-2-Associated X Protein)
RN  - EC 3.4.22.- (Casp3 protein, rat)
RN  - EC 3.4.22.- (Caspase 3)
SB  - IM
MH  - Animals
MH  - Apoptosis/*physiology
MH  - Caspase 3/metabolism
MH  - Disease Models, Animal
MH  - Hyperbaric Oxygenation/*methods
MH  - In Situ Nick-End Labeling
MH  - Ischemic Preconditioning, Myocardial/*methods
MH  - Male
MH  - Myocardial Infarction/metabolism/*pathology/*therapy
MH  - Myocardium/metabolism/pathology
MH  - Neovascularization, Physiologic/physiology
MH  - Proto-Oncogene Proteins c-bcl-2/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - bcl-2-Associated X Protein/metabolism
EDAT- 2010/04/28 06:00
MHDA- 2012/01/10 06:00
CRDT- 2010/04/28 06:00
PHST- 2009/11/18 00:00 [received]
PHST- 2010/01/02 00:00 [revised]
PHST- 2010/01/21 00:00 [accepted]
PHST- 2010/04/28 06:00 [entrez]
PHST- 2010/04/28 06:00 [pubmed]
PHST- 2012/01/10 06:00 [medline]
AID - S0022-4804(10)00085-5 [pii]
AID - 10.1016/j.jss.2010.01.036 [doi]
PST - ppublish
SO  - J Surg Res. 2011 Nov;171(1):41-6. doi: 10.1016/j.jss.2010.01.036. Epub 2010 Feb 
      16.