Failure to protect against myocardial ischemia-reperfusion injury with sevoflurane postconditioning in old rats in vivo

Acta Anaesthesiologica Scandinavica

Volumn 57, Issue 8, 2013, Pages 1024-1031

  Li, H ^a   Zhou, C ^a   Chen, D ^a   Fang, N ^a   Yao, Y ^a   Li, L ^a  

^a PEKING UNION MEDICAL COLLEGE   (China)

Author keywords

[No Author keywords available]

Indexed keywords

2 (2 AMINO 3 METHOXYPHENYL)CHROMONE; 2 MORPHOLINO 8 PHENYLCHROMONE; MITOCHONDRIAL PERMEABILITY TRANSITION PORE; MITOGEN ACTIVATED PROTEIN KINASE 3; MITOGEN ACTIVATED PROTEIN KINASE KINASE 1; NICOTINAMIDE ADENINE DINUCLEOTIDE; PHOSPHATIDYLINOSITOL 3 KINASE; PROTEIN KINASE B; SEVOFLURANE;

ADOLESCENT; AGED; AGING; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CONTROLLED STUDY; ENZYME ACTIVATION; ENZYME PHOSPHORYLATION; GROUPS BY AGE; HEART INFARCTION SIZE; HEART MUSCLE; HEART MUSCLE ISCHEMIA; HEART MUSCLE REPERFUSION; HEART PROTECTION; ISCHEMIC POSTCONDITIONING; NONHUMAN; PRIORITY JOURNAL; RAT; REPERFUSION INJURY; WESTERN BLOTTING;

AGING; ANESTHETICS, INHALATION; ANIMALS; BLOTTING, WESTERN; ENZYME ACTIVATION; ISCHEMIC POSTCONDITIONING; MAP KINASE SIGNALING SYSTEM; METHYL ETHERS; MITOCHONDRIA; MITOGEN-ACTIVATED PROTEIN KINASES; MYOCARDIAL REPERFUSION INJURY; MYOCARDIUM; NAD; PERMEABILITY; PHOSPHORYLATION; PROTO-ONCOGENE PROTEINS C-AKT; RATS; RATS, SPRAGUE-DAWLEY; VENTRICULAR FUNCTION, LEFT;

EID: 84881661834     PISSN: 00015172     EISSN: 13996576     Source Type: Journal    
DOI: 10.1111/aas.12156     Document Type: Article

References (24)

1. Obal D, Scharbatke H, Barthel H, Preckel B, Müllenheim J, Schlack W,. Cardioprotection against reperfusion injury is maximal with only two minutes of sevoflurane administration in rats. Can J Anaesth 2003; 50: 940-945.
2. Obal D, Dettwiler S, Favoccia C, Scharbatke H, Preckel B, Schlack W,. The influence of mitochondrial KATP-channels in the cardioprotection of preconditioning and postconditioning by sevoflurane in the rat in vivo. Anesth Analg 2005; 101: 1252-1260.
3. Deyhimy DI, Fleming NW, Brodkin IG, Liu H,. Anesthetic preconditioning combined with postconditioning offers no additional benefit over preconditioning or postconditioning alone. Anesth Analg 2007; 105: 316-324.
4. Fang NX, Yao YT, Shi CX, Li LH,. Attenuation of ischemia-reperfusion injury by sevoflurane postconditioning involves protein kinase B and glycogen synthase kinase 3 beta activation in isolated rat hearts. Mol Biol Rep 2010; 37: 3763-3769.
5. Pagel PS,. Postconditioning by volatile anesthetics: salvaging ischemic myocardium at reperfusion by activation of prosurvival signaling. J Cardiothorac Vasc Anesth 2008; 22: 753-765.
6. Yao Y, Li L, Li L, Gao C, Shi C,. Sevoflurane postconditioning protects chronically-infarcted rat hearts against ischemia-reperfusion injury by activation of pro-survival kinases and inhibition of mitochondrial permeability transition pore opening upon reperfusion. Biol Pharm Bull 2009; 32: 1854-1861.
7. Housenloy DJ, Tsang A, Mocanu MM, Yellon DM,. Ischemic preconditioning protects by activating prosurvival kinases at reperfusion. Am J Physiol Heart Circ Physiol 2005; 288: H971-976.
8. Housenloy DJ, Tsang A, Yellon DM,. The reperfusion injury salvage kinase pathway: a common target for both ischemic preconditioning and postconditioning. Trends Cardiovasc Med 2005; 15: 69-75.
9. Housenloy DJ, Yellon DM,. reperfusion injury salvage kinase signaling, taking a RISK for cardioprotection. Heart Fail Rev 2007; 12: 217-234.
10. Sniecinski R, Liu H,. Reduced efficacy of volatile anesthetic preconditioning with advanced age in isolated rat myocardium. Anesthesiology 2004; 100: 589-597.
11. Nguyen LH, Rebecchi MJ, Moore LC, Glass PS, Brink PR, Liu L,. Attenuation of isoflurane-induced preconditioning and reactive oxygen species production in the senescent hearts. Anesth Analg 2008; 107: 776-782.
12. Zhu J, Rebecchi MJ, Tan M, Glass PS, Brink PR, Liu L,. Age-associated differences in activation of Akt/GSK-3 singaling pathways and inhibition of mitochondrial permeability transition pore opening in the rat heart. J Gerontol A Biol Sci Med Sci 2010; 65: 611-619.
13. Baines CP,. The mitochondrial permeability transition pore and ischemia-reperfusion injury. Basic Res Cardiol 2009; 104: 181-188.
14. Hausenloy DJ, Yellon DM,. New directions for protecting the heart against ischaemia-perfusion injury: targeting the Reperfusion Injury Salvage Kinase (RISK)-pathway. Cardiovasc Res 2004; 61: 448-460.
15. Przyklenk K, Maynard M, Darling CE, Whittaker P,. Aging mouse hearts are refractory to infarct size reduction with post-conditioning. J Am Coll Cardiol 2008; 51: 1393-1398.
16. Boengler K, Konietzka I, Buechert A, Heinen Y, Garcia-Dorado D, Heusch G, Schulz R,. Loss of ischemic preconditioning's cardioprotection in aged mouse hearts is associated with reduced gap junctional and mitochondrial levels of connexin 43. Am J Physiol Heart Circ Physiol 2007; 292: H1764-1769.
17. Boengler K, Buechert A, Heinen Y, Roeskes C, Hilfiker-Kleiner D, Heusch G, Schulz R,. Cardioprotection by ischemic postconditioning is lost in aged and STAT3-deficient mice. Circ Res 2008; 102: 131-135.
18. Boengler K, Schulz R, Heusch G,. Loss of cardioprotection with aging. Cardiovasc Res 2009; 83: 247-261.
19. Peart JN, Headrick JP,. Clinical cardioprotection and the value of conditioning responses. Am J Physiol Heart Circ Physiol 2009; 296: H1705-1720.
20. Halestrap AP, Clarke SJ, Javadov SA,. Mitochondrial permeability transition pore opening during myocardial reperfusion-a target for cardioprotection. Cardiovasc Res 2004; 61: 372-385.
21. Morin D, Assaly R, Paradis S, Berdeaux A,. Inhibition of mitochondrial membrane permeability as a putative pharmacological target for cardioprotection. Curr Med Chem 2009; 16: 4382-4398.
22. Jiang R, Zatta A, Kin H, Wang N, Reeves JG, Mykytenko J, Deneve J, Zhao ZQ, Guyton RA, Vinten-Johansen J,. PAR-2 activation at the time of reperfusion salvages myocardium via an ERK1/2 pathway in in vivo rat hearts. Am J Physiol Heart Circ Physiol 2007; 293: H2845-2852.
23. Di Lisa F, Menabò R, Canton M, Barile M, Bernardi P,. Opening of the mitochondrial permeability transition pore causes depletion of mitochondrial and cytosolic NAD+ and is a causative event in the death of myocytes in postischemic reperfusion of the heart. J Biol Chem 2001; 276: 2571-2575.
24. Klingenberg M,. Determination of NAD. In:, Bergmeyer HU, Bergmeyer J, Grassl M, eds. Methods of Enzymatic Analysis. Weinheim, Germany: VCH Verlagsgesellschaft, 1986: 253-271.