title: Sevoflurane postconditioning protects isolated rat hearts against ischemia-reperfusion injury: the role of radical oxygen species, extracellular signal-related kinases 1/2 and mitochondrial permeability transition pore.
abstract: The roles of reactive oxygen species (ROS), extracellular signal-regulated kinase 1/2 (ERK 1/2) and mitochondrial permeability transition pore (mPTP) in sevoflurane postconditioning induced cardioprotection against ischemia-reperfusion injury in Langendorff rat hearts were investigated. When compared with the unprotected hearts subjected to 30 min of ischemia followed by 1 h of reperfusion, exposure of 3% sevoflurane during the first 15 min of reperfusion significantly improved functional recovery, decreased infarct size, reduced lactate dehydrogenase and creatine kinase-MB release, and reduced myocardial malondialdehyde production. However, these protective effects were abolished in the presence of either ROS scavenger N-acetylcysteine or ERK 1/2 inhibitor PD98059, and accompanied by prevention of ERK 1/2 phosphorylation and elimination of inhibitory effect on mPTP opening. These findings suggested that sevoflurane postconditioning protected isolated rat hearts against ischemia-reperfusion injury via the recruitment of the ROS-ERK 1/2-mPTP signaling cascade.
authors.affiliation: Department of Anesthesiology, Fuwai Cardiovascular Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, 100037 Beijing, China.
authors.forename: Yun-Tai
authors.initials: YT
authors.lastname: Yao
authors.forename: Li-Huan
authors.initials: LH
authors.lastname: Li
authors.forename: Lei
authors.initials: L
authors.lastname: Chen
authors.forename: Wei-Peng
authors.initials: WP
authors.lastname: Wang
authors.forename: Li-Bing
authors.initials: LB
authors.lastname: Li
authors.forename: Chang-Qing
authors.initials: CQ
authors.lastname: Gao
mesh_terms: D000818:Animals; D006439:Hemodynamics / Q000187:drug effects; D066298:In Vitro Techniques; D048370:MAP Kinase Kinase 2 / Q000378:metabolism*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D008738:Methyl Ethers / Q000494:pharmacology*; D033681:Mitochondrial Membrane Transport Proteins / Q000378:metabolism*; D000083162:Mitochondrial Permeability Transition Pore; D048052:Mitogen-Activated Protein Kinase 3 / Q000378:metabolism*; D009203:Myocardial Infarction / Q000150:complications / Q000473:pathology / Q000503:physiopathology; D009206:Myocardium / Q000201:enzymology / Q000473:pathology*; D009243:NAD / Q000378:metabolism; D010766:Phosphorylation / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism*; D015427:Reperfusion Injury / Q000150:complications / Q000201:enzymology / Q000503:physiopathology / Q000517:prevention & control*; D000077149:Sevoflurane
chemical_list: D008738:Methyl Ethers; D033681:Mitochondrial Membrane Transport Proteins; D000083162:Mitochondrial Permeability Transition Pore; D017382:Reactive Oxygen Species; D009243:NAD; D000077149:Sevoflurane; D008315:Malondialdehyde; D048052:Mitogen-Activated Protein Kinase 3; D048370:MAP Kinase Kinase 2
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