Activation of extracellular signal-regulated kinase after ischemia-reperfusion is required for cardioprotection of sevoflurane-induced preconditioning
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概要
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Brief exposure of volatile anesthetics before prolonged ischemia exerts cardioprotective effects mimicking ischemic preconditioning (Anesthetic preconditioning: APC). We previously reported that in contrast to isoflurane-induced myocardial preconditioning, phosphatidylinositol-3-kinase (PI3K)/Akt signaling, which plays a central role in the reperfusion injury salvage kinase cascade, was not involved in sevoflurane-induced preconditioning. Mitogen-activated protein kinases such as extracellular signal-regulated kinase 1/2 (ERK) and stress-activated protein kinase/c-Jun NH 2-terminal kinase (JNK) have also been implicated in APC. The mitogen-activated protein kinase (MEK)/ERK pathway is another reperfusion salvage kinase pathway in ischemic preconditioning. It remains unclear whether this signaling cascade is involved in sevoflurane-induced preconditioning. Isolated perfused guinea pig hearts were subjected to 30min global ischemia and 120min reperfusion (Control group: CTL). Sevoflurane-induced preconditioning was elicited by administration of sevoflurane for 10min at one minimum alveolar concentration with 10min washout before ischemia (Sevoflurane group: SEVO). Contractile recovery was monitored by left ventricular developed pressure (LVDP) and left ventricular end-diastolic pressure (LVEDP). Infarct size was determined by triphenyltetrazolium chloride stain. Phosphorylation of ERK and JNK were assessed by western blot. After ischemia-reperfusion, SEVO had higher LVDP and lower LVEDP than CTL. Infarct size was significantly reduced in SEVO compared to CTL (42±5% vs 21±6%). Phosphorylation of ERK at 10min after reperfusion was significantly increased compared with CTL. Phosphorylation of JNK was the same for the two groups. The MEK/ERK pathway was more important than PI3/Akt signaling in sevoflurane-induced preconditioning.
- 大阪歯科学会の論文
著者
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Kotani Junichiro
Department of Anesthesiology, Osaka Dental University
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Kotani Junichiro
Osaka Dental Univ. Osaka Jpn
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Kotani J
Department Of Anesthesiology Osaka Dental University
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Kotani Junichiro
Department Of Anesthesiology Osaka Dental University
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Sugioka Shingo
Department Of Anesthesiology Osaka Dental University
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KANEDA Kazuhiro
Department of Applied Physics, Tokyo University of Science
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Okusa Chika
Graduate School, Dentistry (Anesthesiology), Osaka Dental University
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Miyamae Masami
Department of Internal Medicine, Osaka Dental University
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Okusa Chika
Graduate School Dentistry (anesthesiology) Osaka Dental University
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Miyamae Masami
Department Of Internal Medicine Osaka Dental University
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Kaneda Kazuhiro
Department Of Anesthesiology Osaka Dental University
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