| Project/Area Number |
18K15851
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 53020:Cardiology-related
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| Research Institution | Kyushu University |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2023-03-31
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| Project Status |
Completed (Fiscal Year 2022)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2019: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2018: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 急性心不全 / 交感神経 / 血行動態 / 駆出率の低下した心不全 / 心不全 / 動脈圧反射 / 圧受容器反射 |
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| Outline of Final Research Achievements |
Unlike normal animals, animals with heart failure and reduced ejection fraction showed significant pulmonary congestion and reduced cardiac output in a short time after sympathetic nerve activation. These results indicate that sympathetic activation directly contributes to the onset of acute heart failure. The heart failure animals not only had reduced contractility compared to normal animals, but also showed less enhancement of contractility due to sympathetic activation. Sympathetic activation similarly increased afterload in normal and heart failure animals. It is known that increased afterload in heart failure with impaired contractility contributes to congestion and lowers cardiac output, suggesting that increased afterload contributes to exacerbation of heart failure. These findings will lead to the development of novel interventions for acute heart failure.
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| Academic Significance and Societal Importance of the Research Achievements |
駆出率の低下した慢性心不全は急性増悪を繰り返すことが特徴の一つであり、その機序の解明は長らくの課題であった。本研究により交感神経賦活化が直接的に血行動態を悪化させ、急性心不全を発症することを世界で初めて明らかにした。その機序として収縮性の増強不全や心臓エネルギー効率の悪化が関与していることも明らかにした。これらの知見は急性心不全の予防や発症後の最適な治療法の開発につながるものである。全世界で社会問題とされている心不全パンデミック時代において社会的な意義は大きいと考えられる。
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