Ischemic postconditioning inhibits apoptosis after acute myocardial infarction in pigs.

Abstract

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.

• Authors: Haimei Sun, Tao Guo, Liu Liu, Zhuo Yu, Wangbing Xu, Wenhui Chen, Lijuan Shen, Jiaping Wang, Xingkui Dou
• Journal: The heart surgery forum (Heart Surg Forum) Vol. 13 Issue 5 Pg. E305-10 (Oct 2010) ISSN: 1522-6662 [Electronic] United States
• PMID: 20961830 (Publication Type: Comparative Study, Journal Article)

Chemical References

• Proto-Oncogene Proteins c-bcl-2
• bcl-2-Associated X Protein

Topics

• Animals
• Apoptosis
• Blotting, Western
• Disease Models, Animal
• Electrocardiography
• 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)
• Swine
• bcl-2-Associated X Protein (biosynthesis)