| Project/Area Number |
07457167
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Nagoya University |
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Principal Investigator |
ITO Takayuki Nagoya University, School of Medicine Associate Professor, 医学部, 助教授 (10111840)
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| Co-Investigator(Kenkyū-buntansha) |
MURASE Kichiro Nagoya University, School of Medicine Research Fellow, 医学部, 医員
NARUSE Kenshin Nagoya University, School of Medicine Research Fellow, 医学部, 医員
SHINODA Masanori Nagoya University, School of Medicine Research Fellow, 医学部, 医員
TOKI Yukio Nagoya University, School of Medicine Assistant, 医学部, 助手 (20273229)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥6,600,000 (Direct Cost: ¥6,600,000)
Fiscal Year 1996: ¥2,500,000 (Direct Cost: ¥2,500,000)
Fiscal Year 1995: ¥4,100,000 (Direct Cost: ¥4,100,000)
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| Keywords | hypoxia / ischemia / coronary artery / vasodilating factor / factor X / nitric oxide / reactive hyperemia / K channel |
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| Research Abstract |
(1)Hypoxic coronary vasodilatation
We investigated potential involvement of nitric oxide, prostacyclin, adenosine, ATP sensitive K channel-opening in coronary vasodilation during 15 minutes of hypoxia in isolated rat hearts. NO greatly contributes the maintenance of the coronary flow during normoxia (40%). However, NO production is almost completely inhibited during hypoxia. Hypoxia immediately opens the K_<ATP> channels and several minutes later enhances adenosine production, thus relaxing coronary resistant vessels. Reoxygenation also dilates coronary vasculature by opening the K_<Ca> channels.
Reactive hyperemia
To clarify factors other than NO involved in reactive hyperemia after short (30sec) and a long (300sec) coronary global no-flow ischemia in isolated rat hearts. Opening of K_<ATP> channel contributes to coronary vasodilation in reactive hyperemia after short 30-sec ischemia, and opening of K_<Ca>, but not K_<ATP> channel contributes to it after long 300-sec ischemia.
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