2001 Fiscal Year Final Research Report Summary
The effects of hypercapnia, hypocapnia and hypoxia on the coronary flow
| 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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| Keywords | Carbon dioxide / Hypercapnia / Hypocapnia / Hypoxia / Coronary flow / ATP-sensitive potassium channel / Nitric oxide / Endothelium-dependent relaxing factor |
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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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