Document Detail

Ischemic postconditioning inhibits apoptosis after acute myocardial infarction in pigs.
MedLine Citation:
PMID:  20961830     Owner:  NLM     Status:  MEDLINE    
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.
Haimei Sun; Tao Guo; Liu Liu; Zhuo Yu; Wangbing Xu; Wenhui Chen; Lijuan Shen; Jiaping Wang; Xingkui Dou
Publication Detail:
Type:  Comparative Study; Journal Article    
Journal Detail:
Title:  The heart surgery forum     Volume:  13     ISSN:  1522-6662     ISO Abbreviation:  Heart Surg Forum     Publication Date:  2010 Oct 
Date Detail:
Created Date:  2010-10-21     Completed Date:  2011-04-07     Revised Date:  2011-08-05    
Medline Journal Info:
Nlm Unique ID:  100891112     Medline TA:  Heart Surg Forum     Country:  United States    
Other Details:
Languages:  eng     Pagination:  E305-10     Citation Subset:  IM    
Department of ICU, The First Affiliated Hospital of Kunming Medical College, 295 Xin-Chang Road, Kunming, P. R. China.
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MeSH Terms
Blotting, Western
Disease Models, Animal
Follow-Up Studies
Heart Ventricles / metabolism,  pathology*
In Situ Nick-End Labeling
Ischemic Preconditioning, Myocardial / methods*
Myocardial Infarction / metabolism,  pathology,  therapy*
Myocardium / metabolism,  pathology*
Proto-Oncogene Proteins c-bcl-2 / biosynthesis
bcl-2-Associated X Protein / biosynthesis
Reg. No./Substance:
0/Proto-Oncogene Proteins c-bcl-2; 0/bcl-2-Associated X Protein

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