| Project/Area Number |
05670537
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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 |
Respiratory organ internal medicine
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| Research Institution | Tokai University |
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Principal Investigator |
TSUJI Chizuko Tokai University School of Medicine Assistant Professor, 医学部, 講師 (80130079)
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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 |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1994: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1993: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | Oxidant stress / Oxygen radical / MCLA / Perfused lung / Lipopolysaccharide / Lung injury / Hyperoxia / Rat / 活性酸素 / 摘出灌流肺 / ウミホタルルミフェリンアナログ |
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| Research Abstract |
An increased production of oxygen radicals has been postulated to be a major factor in the etiology of so-called oxygen-dependent lung injury (oxydant stress). However, the direct proof for oxygen radicals in oxidant stress has not been clearly shown yet. The purpose of this study was to prove that the oxygen radicals playd a significant role in oxidant stress. We have detected the oxygen radicals by chemiluminescence in the isolated perfused lungs of rats that were injected lipopolysaccharide (a model of ARDS) and were exposed to hyperoxia.
1. lipopolysaccharide (LPS)-induced lung injury : We have measured superoxide production by superoxide-dependent MCLA in isolated perfused rat lungs at 2,6 and 12 hours after LPS injection. We could detect the LPS-induced increase in superoxide production and ability of superoxide production by PMA.Porymorphonuclear leukocyte (PMN) depletion study indicated that PMN was main source of the superoxide. And it was suggested that this method could measure superoxide release and intracellular production simultaneously.
2. hyperoxic lung injury : We could detect an increase in photon counts in no-stimulant condition. This results suggested that large amount of superoxide were continuously produced during hyperoxia. However, these increase in photon counts were not inhibited by SOD.This results showed that the source of the superoxide was not in intravascular space. And isolated PMNs and alveolar macrophages did not increase production of the superoxide. Now we examine the source of the superoxide.
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