1997 Fiscal Year Final Research Report Summary
Gene therapy for acute lung injury
| Project/Area Number |
08671508
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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 |
Thoracic surgery
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| Research Institution | Akita University |
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Principal Investigator |
IZUMI Keiichi Akita University School of Medicine Assistant Professor, 医学部, 講師 (60176237)
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| Co-Investigator(Kenkyū-buntansha) |
MINAMIYA Yoshihiro Akita University School of Medicine Assistant Professor, 医学部, 講師 (30239321)
KITAMURA Michihiko Akita University School of Medicine Associate Professor, 医学部, 助教授 (10153131)
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| Project Period (FY) |
1996 – 1997
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| Keywords | neutrophil / endothelial cell / transendothelial migration |
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| Research Abstract |
It has been reported that reperfusion is the most important factor in ischemia-reperfusion injury. However, causes of ischemia-reperfusion injury in the lung are controversial, because oxygen is always supplied if ventilation continues. Therefore, we hypothesized that nonhypoxic ischemia without reperfusion is sufficient for lung injury. To test our hypothesis, we measured both hydrogen peroxide (H_2O_2)production in the pulmonary circulation by digital imaging fluorescent dichlorofluorescein and the microvascular permeability (MVP) by the Evans blue extravasation technique in the nonhypoxic ischemia rat lung. We made a nonhypoxic ischemia rat lung by clamping the left pulmonary artery. Both H_2O_2 production and MVP increased in the nonhypoxic ischemia rat lung. We also determined the effect of oxygen removal by clamping bronchus in advance of pulmonary artery occlusion, intercellular adhesion molecule-1 (ICAM-1) neutralization with monoclonal antibody 1A29, and plateletactivating factor (PAF) receptor antagonist CV6209 on H_2O_2 production and MVP.These treatmrnts inhibited both H_2O_2 production and MVP increase. At high power viewing of the fluorescent dichlorofluorescein image, H_2O_2 was detected in the leukocytes within pulmonary capillaries. These data indicate that the nonhypoxic ischemia without reperfusion alone causes radical production and increases MVP.Furthermore, PAF and ICAM-1 contribute to these reactions.
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