| Project/Area Number |
12671481
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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 | OITA MEDICAL UNIVERSITY |
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Principal Investigator |
NOGUCHI Takayuki OITA MEDICAL UNIVERSITY, DEPT. OF ANESTHESIOLOGY, PROFESSOR, 医学部, 教授 (90156183)
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| Co-Investigator(Kenkyū-buntansha) |
MORI Masakazu OITA MEDICAL UNIVERSITY, LECTURER, 医学部, 講師 (20220022)
KIRA Shinitiro OITA MEDICAL UNIVERSITY, STUDENT IN DOCTOR COURSE
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2001: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2000: ¥2,600,000 (Direct Cost: ¥2,600,000)
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| Keywords | lung injury / mild hypothermia / ntercellular / adhesion molecule-1 / acute respiratory distress syndrome / 好中球 / 接着分子 / ICAM-1 |
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| Research Abstract |
The pathophysiology of the acute phase of acid-induced lung injury has been elucidated. However, once acute respiratory distress syndrome (ARDS) develops, the mortality rate remains high and there is, as yet, no effective therapy. There are reports that application of mild hypothermia is an effective treatment for ARDS, but, at the tissue and the molecular level, there is no clear understanding of the factors that to the positive outcome of such treatment. We studied the effects of mild hypothermia on the expression of intercellular adhesion molecule-1 (ICAM-1) and the accumulation of neutrophils after acid-induced lung injury in the rat. Oxygenation in acid-instilled rats was significantly impaired as compared to that in non-instilled groups, but induction of mild hypothermia gradually improved oxygenation. Expression of ICAM-1 was enhanced in the acid-instilled normothermic group. By contrast, no overexpression of ICAM-1 and its transcript was detected in the acid-instilled hypothermic group. In addition, accumulation of neutrophils was markedly inhibited after exposure to mild hypothermia irrespective of the instillation of acid. Our data suggest that mild hypothermia can inhibit the adhesion, activation, and accumulation of neutrophils in the acute phase of acid-induced lung injury and suggest an approach that might potentially reduce ongoing damage in patients with ARDS.
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