A new calpain inhibitor protects left ventricular dysfunction induced by mild ischemia-reperfusion in in situ rat hearts.

• Material Type: 博士論文
• Title: A new calpain inhibitor protects left ventricular dysfunction induced by mild ischemia-reperfusion in in situ rat hearts.
• Author/Editor: Takeshita, Daisuke; Tanaka, Midori; Mitsuyama, Shinichi; Yoshikawa, Yoshirou; Zhang, Guo-Xing; Obata, Koji; Ito, Haruo; Taniguchi, Shigeki; Takaki, Miyako
• Author Heading: Takeshita, Daisuke; Tanaka, Midori; Mitsuyama, Shinichi; Yoshikawa, Yoshirou; Zhang, Guo-Xing; Obata, Koji; Ito, Haruo; Taniguchi, Shigeki; Takaki, Miyako
• Publication, Distribution, etc.: Springer Japan / Physiological Society of Japan
• Publication Date: 2013-03
• Publication Date (W3CDTF): 2013-03
• Alternative Title: 新しいカルパイン阻害剤はラット生体位心における緩和な虚血再灌流による左心室機能障害を保護する
• Periodical title: The journal of physiological sciences
• No. or year of volume/issue: 63 2
• Volume: 63
• Issue: 2
• Pages: 113-123
• ISSN (Periodical Title): ISSN : 1880-6546
• Degree grantor/type: 奈良県立医科大学
• Date Granted: 2014-03-17
• Dissertation Number: 甲第617号
• Degree Type: 博士（医学）
• Text Language Code: eng
• Subject Heading: Mild ischemic-reperfusion injury; Cardioprotection; α-Fodrin; SNJ-1945
• Target Audience: 一般
• Note (General): type:Thesis; We have previously indicated that a new soluble calpain inhibitor, SNJ-1945 (SNJ), attenuates cardiac dysfunction after cardioplegia arrest-reperfusion by inhibiting the proteolysis of α-fodrin in in vitro study. Nevertheless, the in vivo study design is indispensable to explore realistic therapeutic approaches for clinical use. The aim of the present in situ study was to investigate whether SNJ attenuated left ventricular (LV) dysfunction (stunning) after mild ischemic-reperfusion (mI-R) in rat hearts. SNJ (60 μmol/l, 5 ml i.p.) was injected 30 min before gradual and partial coronary occlusion at proximal left anterior descending artery. To investigate LV function, we obtained curvilinear end-systolic pressure–volume relationship by increasing afterload 60 min after reperfusion. In the mI-R group, specific LV functional indices at midrange LV volume (mLVV), end-systolic pressure (ESPmLVV), and pressure–volume area (PVAmLVV: a total mechanical energy per beat, linearly related to oxygen consumption) significantly decreased, but SNJ reversed these decreases to time control level. Furthermore, SNJ prevented the α-fodrin degradation and attenuated degradation of Ca2+ handling proteins after mI-R. Our results indicate that improvements in LV function following mI-R injury are associated with inhibition of the proteolysis of α-fodrin in in situ rat hearts. In conclusion, SNJ should be a promising tool to protect the heart from the stunning.; 博士（医学）・甲617号・平成26年3月17日; identifier:The journal of physiological sciences Vol.63 No.2 p.113-123; identifier:18806546; identifier:http://ginmu.naramed-u.ac.jp/dspace/handle/10564/2702; identifier:The journal of physiological sciences, 63(2): 113-123
• Source: fulltext; http://ginmu.naramed-u.ac.jp/dspace/bitstream/10564/2702/1/01%e6%9c%ac%e6%96%87%e3%81%ae%e8%a6%81%e6%97%a8.pdf; http://ginmu.naramed-u.ac.jp/dspace/bitstream/10564/2702/2/02%e5%af%a9%e6%9f%bb%e8%a6%81%e6%97%a8.pdf; http://ginmu.naramed-u.ac.jp/dspace/bitstream/10564/2702/3/03%e6%9c%ac%e6%96%87.pdf
• Access Restrictions: インターネット公開
• Related Material (DOI): 10.1007/s12576-012-0243-6
• Periodical Title (NCID): AA12129145; https://ci.nii.ac.jp/ncid/AA12129145
• Data Provider (Database): 国立情報学研究所 : 学術機関リポジトリデータベース（IRDB）（機関リポジトリ）; https://irdb.nii.ac.jp
• Original Data Provider (Database): 奈良県立医科大学 : 奈良県立医科大学機関リポジトリ GINMU