PMID- 20961830
OWN - NLM
STAT- MEDLINE
DCOM- 20110407
LR  - 20240104
IS  - 1522-6662 (Electronic)
IS  - 1098-3511 (Linking)
VI  - 13
IP  - 5
DP  - 2010 Oct
TI  - Ischemic postconditioning inhibits apoptosis after acute myocardial infarction in 
      pigs.
PG  - E305-10
LID - 10.1532/HSF98.20101013 [doi]
AB  - OBJECTIVES: Recent studies have shown that ischemic postconditioning reduces 
      myocardial ischemia-reperfusion (I/R) injury; however, the effects of inhibiting 
      apoptosis on cardioprotection induced by ischemic postconditioning remain to be 
      determined. The objective of this study was to investigate whether ischemic 
      postconditioning attenuates myocardial I/R injury by reduced apoptosis in a 
      closed-chest pig model of acute myocardial infarction. METHODS: Diannan small-ear 
      pigs were randomly divided into 3 groups (5/group): (1) The sham group underwent 
      a sham operation without ischemia; (2) the I/R group received 60 minutes of 
      ischemia and 72 hours of reperfusion; and (3) the ischemic postconditioning 
      (Postcond) group was treated the same as the I/R group except that the pigs 
      received 8 cycles of 30 seconds of reperfusion and 30 seconds of ischemia at the 
      onset of reperfusion. After 72 hours of reperfusion, infarct size was measured by 
      2,3,5-triphenyltetrazolium chloride staining. Apoptotic cells in the peri-infarct 
      myocardium were evaluated with the terminal deoxynucleotidyl transferase-mediated 
      dUTP nick end labeling (TUNEL) method, and apoptosis-related molecules were 
      studied with western blotting analysis. RESULTS: After 72 hours of reperfusion, 
      mean (+/-SEM) infarct size was significantly smaller in the Postcond group than in 
      the I/R group (23.26% +/- 3.13% versus 10.89% +/- 2.02%, P < .05). Apoptotic myocytes 
      in the peri-infarct region were lower in the Postcond group than in the I/R group 
      (15.31% +/- 4.58% versus 33.83% +/- 4.44%, P < .05). This decrease in the extent of 
      apoptosis was accompanied by a significant decrease in Bax expression (0.306 +/- 
      0.075 versus 0.433 +/- 0.102 for the I/R group; P < .05) and a significant increase 
      in Bcl-2 expression (1.801 +/- 0.227 versus 1.267 +/- 0.308 for the I/R group; P < 
      .05). CONCLUSIONS: In a clinically relevant closed-chest pig model of myocardial 
      infarction, these data suggest the following: (1) Ischemic postconditioning 
      reduces infarct size following prolonged reperfusion, and (2) this 
      cardioprotective effect is likely achieved via antiapoptotic mechanisms.
FAU - Sun, Haimei
AU  - Sun H
AD  - Department of ICU, The First Affiliated Hospital of Kunming Medical College, 295 
      Xin-Chang Road, Kunming, P. R. China.
FAU - Guo, Tao
AU  - Guo T
FAU - Liu, Liu
AU  - Liu L
FAU - Yu, Zhuo
AU  - Yu Z
FAU - Xu, Wangbing
AU  - Xu W
FAU - Chen, Wenhui
AU  - Chen W
FAU - Shen, Lijuan
AU  - Shen L
FAU - Wang, Jiaping
AU  - Wang J
FAU - Dou, Xingkui
AU  - Dou X
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PL  - United States
TA  - Heart Surg Forum
JT  - The heart surgery forum
JID - 100891112
RN  - 0 (Proto-Oncogene Proteins c-bcl-2)
RN  - 0 (bcl-2-Associated X Protein)
SB  - IM
MH  - Animals
MH  - *Apoptosis
MH  - Blotting, Western
MH  - Disease Models, Animal
MH  - Electrocardiography
MH  - Follow-Up Studies
MH  - Heart Ventricles/metabolism/*pathology
MH  - In Situ Nick-End Labeling
MH  - Ischemic Preconditioning, Myocardial/*methods
MH  - Myocardial Infarction/metabolism/pathology/*therapy
MH  - Myocardium/metabolism/*pathology
MH  - Proto-Oncogene Proteins c-bcl-2/biosynthesis
MH  - Swine
MH  - bcl-2-Associated X Protein/biosynthesis
EDAT- 2010/10/22 06:00
MHDA- 2011/04/08 06:00
CRDT- 2010/10/22 06:00
PHST- 2010/10/22 06:00 [entrez]
PHST- 2010/10/22 06:00 [pubmed]
PHST- 2011/04/08 06:00 [medline]
AID - AQN776668W863181 [pii]
AID - 10.1532/HSF98.20101013 [doi]
PST - ppublish
SO  - Heart Surg Forum. 2010 Oct;13(5):E305-10. doi: 10.1532/HSF98.20101013.