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Sevoflurane induces cardioprotection through reactive oxygen species-mediated upregulation of autophagy in isolated guinea pig hearts
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  • 作者:Mayumi Shiomi (1)
    Masami Miyamae (2)
    Genzou Takemura (3)
    Kazuhiro Kaneda (4)
    Yoshitaka Inamura (4)
    Anna Onishi (4)
    Shizuka Koshinuma (4)
    Yoshihiro Momota (4)
    Toshiaki Minami (1)
    Vincent M. Figueredo (5)
  • 关键词:Sevoflurane ; Preconditioning ; Autophagy ; Ischemia–reperfusion ; Reactive oxygen species
  • 刊名:Journal of Anesthesia
  • 出版年:2014
  • 出版时间:August 2014
  • 年:2014
  • 卷:28
  • 期:4
  • 页码:593-600
  • 全文大小:689 KB
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  • 作者单位:Mayumi Shiomi (1)
    Masami Miyamae (2)
    Genzou Takemura (3)
    Kazuhiro Kaneda (4)
    Yoshitaka Inamura (4)
    Anna Onishi (4)
    Shizuka Koshinuma (4)
    Yoshihiro Momota (4)
    Toshiaki Minami (1)
    Vincent M. Figueredo (5)

    1. Department of Anesthesiology, Osaka Medical College, Takatsuki, Japan
    2. Department of Internal Medicine, Osaka Dental University, 8-1 Kuzuha hanazono-cho Hirakata, Osaka, 573-1121, Japan
    3. Department of Cardiology, Gifu University Graduate School of Medicine, Gifu, Japan
    4. Department of Anesthesiology, Osaka Dental University, Osaka, Japan
    5. Institute for Heart and Vascular Health, Einstein Medical Center, Jefferson Medical College, Philadelphia, USA
  • ISSN:1438-8359
文摘
Purpose Sevoflurane increases reactive oxygen species (ROS), which mediate cardioprotection against myocardial ischemia–reperfusion injury. Emerging evidence suggests that autophagy is involved in cardioprotection. We examined whether reactive oxygen species mediate sevoflurane preconditioning through autophagy. Methods Isolated guinea pigs hearts were subjected to 30?min ischemia followed by 120?min reperfusion (control). Anesthetic preconditioning was elicited with 2?% sevoflurane for 10?min before ischemia (SEVO). The ROS-scavenger, N-(2-mercaptopropionyl) glycine (MPG, 1?mmol/l), was administered starting 30?min before ischemia to sevoflurane-treated (SEVO?+?MPG) or non-sevoflurane-treated (MPG) hearts. Infarct size was determined by triphenyltetrazolium chloride stain. Tissue samples were obtained after reperfusion to determine autophagy-related protein (microtubule-associated protein light chain I and II: LC3-I, -II) and 5-AMP-activated protein kinase (AMPK) expression using Western blot analysis. Electron microscopy was used to detect autophagosomes. Results Infarct size was significantly reduced and there were more abundant autophagosomes in SEVO compared with control. Western blot analysis revealed that the ratio of LC3-II/I and phosphorylation of AMPK were significantly increased in SEVO. These effects were abolished by MPG. Conclusions Sevoflurane induces cardioprotection through ROS-mediated upregulation of autophagy.

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