Isoflurane-induced postconditioning via mitochondrial calcium-activated potassium channels 1-2

• Material Type: 博士論文
• ISSN: 1349-6867
• Title: Isoflurane-induced postconditioning via mitochondrial calcium-activated potassium channels
• Volume: 63 1-2
• Author/Editor: Kinoshita, Michiko; Tsutsumi, Yasuo M.; Fukuta, Kohei; Kasai, Asuka; Tanaka, Katsuya
• Author Heading: Kinoshita, Michiko; Tsutsumi, Yasuo M.; Fukuta, Kohei; Kasai, Asuka; Tanaka, Katsuya
• Publication, Distribution, etc.: Faculty of Medicine Tokushima University
• Publication Date: 2016-02
• Publication Date (W3CDTF): 2016-02
• Alternative Title: イソフルラン誘発性のポストコンディショニング効果はミトコンドリアのカルシウム依存性カリウムチャネルを介している; Isoflurane actions via the mKCa channel
• Periodical title: The Journal of Medical Investigation
• Degree grantor/type: 徳島大学
• Date Granted: 2016-03-22
• Date Granted (W3CDTF): 2016-03-22
• Dissertation Number: 甲第2948号
• Degree Type: 博士（医学）
• Conferring No. (Dissertation): 甲第2948号
• Text Language Code: eng
• Subject Heading: Mitochondrial calcium-activated potassium channel; Anesthetic-induced postconditioning; Isoflurane
• Target Audience: 一般
• Note (General): Purpose : Activation of the mitochondrial calcium-activated potassium (mKCa) channel reportedly confers resistance to myocardial ischemic stress. However, the role of the mKCa channel in postconditioning induced by volatile anesthetic remains unclear. Methods :Male Japanese white rabbits underwent coronary artery occlusion for 30 min followed by reperfusion for 3 h. Volatile anesthetic, isoflurane, was administered at 3min prior to reperfusion for 5 min. Rabbits were injected with the mKCa channel blocker, iberiotoxin, or the mKCa channel opener, NS1619, at 8 min prior to reperfusion. Myocardial infarct size and the area at risk (AAR) were measured at the end of the experiment. Results : Isoflurane significantly reduced infarct size (23.0±9.8% of the AAR, P<0.05) compared with the control (44.0±9.1%). Iberiotoxin abolished the cardioprotective impact of isoflurane (43.0±11.6%), while iberiotoxin alone exerted no effect on infarct size (45.0±9.5%). NS1619 and isoflurane/ NS1619 both significantly reduced infarct size (21.0±10.3% and 19.0±8.8%, respectively, P<0.05 vs control group), but isoflurane/NS1619 showed no additional benefits compared with isoflurane alone. Conclusion : These results indicate that activation of the mKCa channel contribute isoflurane-induced postconditioning.
• DOI: info:doi/10.2152/jmi.63.80; https://doi.org/info:doi/10.2152/jmi.63.80
• Persistent ID (NDL): info:ndljp/pid/10121027; https://dl.ndl.go.jp/pid/10121027
• Collection: 障害者向け資料
• Collection (Materials For Handicapped People:1): テキストデータ
• Collection (particular): 国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文; https://dl.ndl.go.jp/collections/A00014
• Acquisition Basis: 博士論文（自動収集）
• Date Accepted (W3CDTF): 2016-07-07T04:28:02+09:00
• Format (IMT): application/pdf
• Access Restrictions: 国立国会図書館内限定公開
• Service for the Digitized Contents Transmission Service: 図書館・個人送信対象外
• Availability of remote photoduplication service: 可
• Periodical Title (URI): https://repo.lib.tokushima-u.ac.jp/111158
• Data Provider (Database): 国立国会図書館 : 国立国会図書館デジタルコレクション; https://dl.ndl.go.jp

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2019-09-09 再収集