| Project/Area Number |
05671118
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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 |
Thoracic surgery
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| Research Institution | Osaka University |
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Principal Investigator |
SAWA Yoshiki Osaka University Medical Assistant, 医学部, 助手 (00243220)
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| Co-Investigator(Kenkyū-buntansha) |
FUKUSHIMA Norihide Osaka University Medical Assistant, 医学部, 助手 (30263247)
KADOBA Keishi Osaka University Medical Assistant, 医学部, 助手 (00185886)
西村 元延 大阪大学, 医学部・附属病院, 医員
大竹 重彰 大阪大学, 医学部, 助手 (50243209)
金香 充範 大阪大学, 医学部, 助手 (70169580)
中埜 粛 大阪大学, 医学部, 講師 (70028653)
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| Project Period (FY) |
1993 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
|
| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1994: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1993: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | Myocyte / Endothelial cell / reperfusion injury / Neutrophil / complement / reperfusiou injuvy / complement / Endothelial Cell / reperfusion injury / Complement |
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| Research Abstract |
The present study was designed to elucidate the role of Nitric Oxide(NO) in ischemia-reperfusion induced endothelial injury in view of vascular permeability and neutrophil activation. Microvascular endothelial cells and neutrophils were isolated from adult rat heart and blood. We measured the transmembrane FITC-albumin leakage as indices of permeability, chemiluminescence value and neutrophil adherence to endothelial cell(%). Permeability was increased by addition of neutrophils during reoxygenation after 6 hours hypoxia. L-arginine and Nitroprusside decreased microvascular permeability by inhibiting neutrophil activation and adhesion to endothelial cell. These results indicate that decrease of constitutive NO release from endothelial cell after ischemia may cause the increase of permeability, adherence and activation of neutrophils resulting in enhancement of endothelial injury.
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