| Project/Area Number |
25460281
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
General physiology
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| Research Institution | Akita University |
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Principal Investigator |
ONO Kyoichi 秋田大学, 医学(系)研究科(研究院), 教授 (70185635)
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| Co-Investigator(Kenkyū-buntansha) |
OHBA Takayoshi 秋田大学, 大学院医学系研究科, 助教 (80431625)
SHIBATA Shigehiro 秋田大学, 大学院医学系研究科, 講師 (10326671)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 心房細動 / 肺静脈 / 自動能 / 不整脈 / イオンチャネル / Clチャネル / ペーシング / リモデリング |
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| Outline of Final Research Achievements |
Extensions of striated myocardium from the left atrium into the pulmonary veins (PVs) are termed myocardial sleeves. Ectopic activity of cardiomyocytes in the sleeves is thought to be responsible for initiation and maintenance of atrial fibrillation, the most frequent sustained arrhythmia encountered in clinical practice. We have reported that PV cardiomyocytes have the potential to generate spontaneous activity. In this study, we found a novel hyperpolarizing-activated Cl- current in PV cardiomyocytes, not in atrial and ventricular myocytes. We also showed that the norepinephrine-induced automaticity could be stopped by Cl- channel blocker, indicating that IClh may play a functional role in the NE-induced automaticity. Furthermore, a computer simulation model was constructed to reconstruct electrical activity of PV cardiomyocytes, and electrical remodeling of rat atrial myocytes using rapid atrial pacing were analyzed.
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