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 |
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Authors: | Yun-Tai Yao Li-Huan Li Lei Chen Wei-Peng Wang Li-Bing Li Chang-Qing Gao |
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Institution: | (1) Department of Anesthesiology, Fuwai Cardiovascular Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, 100037 Beijing, China;(2) Department of Cardiovascular Surgery and Cardiovascular Institute, General Hospital of the People’s Liberation Army, 100853 Beijing, China;(3) No. 167 Beilishi Road, 100037 Xicheng District, Beijing, China; |
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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. |
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