| Project/Area Number |
05671259
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | Mie University |
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Principal Investigator |
MARUYAMA Kazuo Mie University, University Hospital, Lecturer, 医学部・付属病院, 講師 (20181828)
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| Co-Investigator(Kenkyū-buntansha) |
MUNEYUKI Mannosuke Mie University, Faculty of Medicine, Professor, 医学部, 教授 (50077583)
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| Project Period (FY) |
1993 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1994: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1993: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | nitric oxide / pulmonary hyperfension / inhalation / 肺血管病変 |
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| Research Abstract |
Nitric oxide (NO) released from endothelium plays an important role in regulating vascular tone. No may be released from intramural nerve endings from nonadrenergic, noncholinergic nerve and this also leads to vasodilation. In pulmonary hypertension endothelial changes and hypertropy and hyperplasia in vascular smooth muscles in the media are observed. In hypertensive pulmonary areies, endothelium-dependent relaxation induced by acetylcholine and relaxation induced by NO were impaired. This might due to desensitization of soluble guanylate cyclase in the pulmonary vasular smooth muscle, because there may be an increase in nitric oxide production in endothelium of hypertensive pulmonary arteries. Although relaxation to NO is depressed compared to control, the relaxant effect of NO is not completely abolished. In pulmonary hypertensive rats with structural remodeling inhaled NO did induced selective pulmonary vasodilatation.
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