Ischemic Postconditioning Protects Elderly Rat Hearts against Ischemia-reperfusion Injury via P-Akt Signaling Pathway_Chinese Journal of Clinical Thoracic and Cardiovascular Surgery

Authors：

WANG Bo , TAO Liang , CHEN Xufa , FENG Xueguo.

Department of Cardiac Surgery， Wuhan Asia Heart Hospital， Wuhan 430022， P. R. China;

Corresponding author：

Keywords：

Ischemic postconditioning; 　Cardioprotection; 　Ischemia-reperfusion; 　Phosphorylated Akt

DOI：

10.7507/1007-4848.20130216

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Objective To explore the impact of ischemic postconditioning on ischemia-reperfusion injury in isolatedelderly rat hearts and their relation with P-Akt. Methods A total of 30 healthy elderly SD rats (21-23 months old， male or female) with their body weight of 450-500 g were divided into 3 groups: control group， ischemia-reperfusion group， and postconditioning group， with 10 rats in each group. Coronary artery blood flow，myocardial infarction size， phosphorylatedAkt （p-Akt） expression， and changes in myocardium and mitochondria were detected. Results Coronary artery blood flow of the postconditioning group was significantly higher than that of the ischemia-reperfusion group （6.4±1.2 ml/min vs.3.1±1.2 ml/min， P＜0. 01）， and myocardial infarction size of the postconditioning group was significantly smaller thanthat of the ischemia-reperfusion group （35.0%±2.0% vs. 55.7%±3.6%， P lt;0. 05）. The expression of P-Akt was significantlyhigher， and myocardial fibers and mitochondria were preserved better in the postconditioning group than the ischemia-reperfusion group. Conclusion Ischemic postconditioning can protect isolated elderly rat hearts against ischemia-reperfusion injury， which may be related to P-Akt activation.

Citation： WANG Bo,TAO Liang,CHEN Xufa,FENG Xueguo.. Ischemic Postconditioning Protects Elderly Rat Hearts against Ischemia-reperfusion Injury via P-Akt Signaling Pathway. Chinese Journal of Clinical Thoracic and Cardiovascular Surgery, 2013, 20(6): 710-713. doi: 10.7507/1007-4848.20130216 Copy

1.	王波，闫德民，陶凉. 缺血后处理对糖尿病大鼠再灌注心肌的保护作用及其与P-AKT的关系. 中华胸心血管外科杂志， 2010， 26 （3）：193-196.
2.	阎德民，王伟，王波. 温度对PGC-1在心肌细胞中的表达的影响. 中国医科大学学报， 2008， 37 （1）：38-40.
3.	彭龙云，马虹，何建桂，等. 缺血后处理减轻大鼠肥厚心肌缺血再灌注损伤的观察. 中华心血管病杂志， 2006， 34 （8）：685-689.
4.	Zhao ZQ， Corvera JS， Halkos ME， et al. Inhibition of myocardial injury by ischemic postconditioning during reperfusion：comparison with ischemic preconditioning. Am J Physiol Heart Circ Physiol， 2003， 285 （2）：H579-588.
5.	Kerendi F， Kin H， Halkos ME， et al. Remote postconditioning. Brief renal ischemia and reperfusion applied before coronary artery reperfusion reduces myocardial infarct size via endogenous activation of adenosine receptors.Basic Res Cardiol， 2005， 100 （5）：404-412.
6.	Kin H， Zatta AJ， Lofye MT， et al. Postconditioning reduces infarct size via adenosine receptor activation by endogenous adenosine. Cardiovasc Res， 2005， 67 （1）：124-133.
7.	Bopassa JC， Ferrera R， Gateau-Roesch O， et al. Couture——kepetit and M. Ovize， PI 3-kinase regulates the mitochondrial transition pore in controlled reperfusion and postconditionig. Cardiovas Res， 2006， 69 （1）：178-185.
8.	Darling CE， Jiang R， Maynard M， et al. Postconditioning via stutteringreperfusion 1imits myocardial infarct size in rabbit heart：role of ERK1/2. Am J Physiol Heart Circ Physiol， 2005， 289：1618-1626.
9.	Yang XM， Proctor JB， Cui L， et al. Multiple， brief coronary occlusions during early reperfusion protect rabbit hearts by targeting cell signaling pathways. J Am Coil Cardiol， 2004 ，44：1103-1110.
10.	Yang XM， Philipp S， Downey JM， et al. Postconditioning's protection is not dependent on circulating blood factors or cells but involves adenosine receptors and requires PI3-kinase and guanylyl cyclase activation. BasicRes Cardio1， 2005， 100 （1）：57-63.
11.	Zatta AJ， Kin H， Lee G， et al. Infarct-sparing effect of myocardialpostconditioning is dependent on protein kinase C signalling. Cardiovasc Res， 2006， 70 （2）：315-324.
12.	Argaud L， Gateau-Roesch O， Raisky O， et al. Postconditioninginhibits mitechondrial permeability transition. Circulation， 2005， 111 （2）：194-197.
13.	Feng J， Lucchinetti E， Ahuja P， et al. Isoflurane postconditioning prevents opening of the mitochondrial permeability transition pore through inhibition of glycogen synthase kinase 3beta. Anesthesiology，2005， 103 （5）：987-995.

1. 　王波，闫德民，陶凉. 缺血后处理对糖尿病大鼠再灌注心肌的保护作用及其与P-AKT的关系. 中华胸心血管外科杂志， 2010， 26 （3）：193-196.
2. 　阎德民，王伟，王波. 温度对PGC-1在心肌细胞中的表达的影响. 中国医科大学学报， 2008， 37 （1）：38-40.
3. 　彭龙云，马虹，何建桂，等. 缺血后处理减轻大鼠肥厚心肌缺血再灌注损伤的观察. 中华心血管病杂志， 2006， 34 （8）：685-689.
4. 　Zhao ZQ， Corvera JS， Halkos ME， et al. Inhibition of myocardial injury by ischemic postconditioning during reperfusion：comparison with ischemic preconditioning. Am J Physiol Heart Circ Physiol， 2003， 285 （2）：H579-588.
5. 　Kerendi F， Kin H， Halkos ME， et al. Remote postconditioning. Brief renal ischemia and reperfusion applied before coronary artery reperfusion reduces myocardial infarct size via endogenous activation of adenosine receptors.Basic Res Cardiol， 2005， 100 （5）：404-412.
6. 　Kin H， Zatta AJ， Lofye MT， et al. Postconditioning reduces infarct size via adenosine receptor activation by endogenous adenosine. Cardiovasc Res， 2005， 67 （1）：124-133.
7. 　Bopassa JC， Ferrera R， Gateau-Roesch O， et al. Couture——kepetit and M. Ovize， PI 3-kinase regulates the mitochondrial transition pore in controlled reperfusion and postconditionig. Cardiovas Res， 2006， 69 （1）：178-185.
8. 　Darling CE， Jiang R， Maynard M， et al. Postconditioning via stutteringreperfusion 1imits myocardial infarct size in rabbit heart：role of ERK1/2. Am J Physiol Heart Circ Physiol， 2005， 289：1618-1626.
9. 　Yang XM， Proctor JB， Cui L， et al. Multiple， brief coronary occlusions during early reperfusion protect rabbit hearts by targeting cell signaling pathways. J Am Coil Cardiol， 2004 ，44：1103-1110.
10. 　Yang XM， Philipp S， Downey JM， et al. Postconditioning's protection is not dependent on circulating blood factors or cells but involves adenosine receptors and requires PI3-kinase and guanylyl cyclase activation. BasicRes Cardio1， 2005， 100 （1）：57-63.
11. 　Zatta AJ， Kin H， Lee G， et al. Infarct-sparing effect of myocardialpostconditioning is dependent on protein kinase C signalling. Cardiovasc Res， 2006， 70 （2）：315-324.
12. 　Argaud L， Gateau-Roesch O， Raisky O， et al. Postconditioninginhibits mitechondrial permeability transition. Circulation， 2005， 111 （2）：194-197.
13. 　Feng J， Lucchinetti E， Ahuja P， et al. Isoflurane postconditioning prevents opening of the mitochondrial permeability transition pore through inhibition of glycogen synthase kinase 3beta. Anesthesiology，2005， 103 （5）：987-995.

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Ischemic Postconditioning Protects Elderly Rat Hearts against Ischemia-reperfusion Injury via P-Akt Signaling Pathway

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