| Project/Area Number |
18K08058
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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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| Review Section |
Basic Section 53020:Cardiology-related
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| Research Institution | Hokkaido University |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2020: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 光遺伝学 / 心室細動 / 心室性不整脈 / 心房細動 |
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| Outline of Final Research Achievements |
We initially aimed to explore the roll of purkinje-myocardial junction in the initiation and maintenance of ventricular fibrillation. However, we could not complete this research. We consider the major reason of our failure was that it was quite challenging to manage the light emission onto PMJ because the mouse heart was tiny. Experimental approach using bigger animal might resolve this problem.
With the failure of the initial research plan, we shifted our research theme to light termination of atrial fibrillation (AF). We successfully terminated AF in the heart of Tg mouse with channelrhodopsin 2 in cell expressing connexin 40. We, for the first time, observed the prolongation of action potential duration (APD) using optical mapping. We continue this project and are aiming to investigate the relationship between light-induced change of the physiological parameters and the termination rate of AF.
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| Academic Significance and Societal Importance of the Research Achievements |
当初の目的とは異なる実験を展開することになったが、vivoレベルでは、チャネルロドプシンの刺激による活動電位持続時間（APD)の延長効果はこれまでに証明されておらず、今回の研究で初めて、マウスの還流心でのAPD延長を確認した。今後、光照射の種々のパラメータ（照射時間、範囲、光強度など）と心房細動停止率との関係性を今後明らかにすることで、より効率的な光除細動を行うことが可能になると期待される。
将来的に光除細動治療の発展につながる基盤的知見を得ることができた。
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