| Project/Area Number |
11671516
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | Yokohama City University |
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Principal Investigator |
OKAZAKI Kaoru Department of Anesthesiology Yokohama City University, School of Medicine Associate Professor, 医学部附属病院, 講師 (80160662)
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| Co-Investigator(Kenkyū-buntansha) |
ENDOU Masayuki Department of Anesthesiology Yokohama City University, School of Medicine Associate Professor, 医学部附属病院, 講師 (90244508)
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| Project Period (FY) |
1999 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2001: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2000: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1999: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | Carbon dioxide / Hypercapnia / Hypocapnia / Hypoxia / Coronary flow / ATP-sensitive potassium channel / Nitric oxide / Endothelium-dependent relaxing factor / 高二酸化炭素分圧 / 低酸素分圧 / 内皮依存性冠血管拡張作用 / 一酸化窒素 / 冠動脈内皮障害 / 低二酸化炭素分圧 / 内皮非依存性冠血管拡張作用 |
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| Research Abstract |
The purpose of the present study is to clarify the effects of hypocapnia, hypocapnia, hypercapnia and hypoxia on the coronary flow before and after the disruption of NOS activity of ATP-sensitive K+(KATP) channel activity in the isolated guinea pig heart.
Denudation of the coronary endothelium with CHAPS or the presence of nitric oxide synthase(NOS) inhibitor, 0.3 mM Nω-Nitro-L-Arginine (NNA) attenuated significantly hypercapnia-produced increase in the coronary flow, whereas it potentiated significantly hypocapnia-produced decrease in the coronary flow. When both NOS and KATP channel were blocked by NNA and 5microM glibenclamide(GLIB), the hypercapnia-produced increase and the hypocapnia-produced decrease were abolished completely.
The presence of NNA, or GLIB did not attenuate significantly the hypoxia-produced increase in the coronary flow, whereas sumiltaneous presence of both NNA and GLIB attenuated significantly the hypoxia-produced increase in the coronary flow.
The present study suggests that EDRF(endothelial-dependent relaxing factor) and KATP channel are included in the mechanism in the effects of carbon dioxide, or hypoxia on the coronary flow.
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