1999 Fiscal Year Final Research Report Summary
Study of the mechanism of lung vascular permeability in pulmonary edema
| Project/Area Number |
09470325
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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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 | NAGOYA UNIVERSITY |
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Principal Investigator |
SHIMADA Yasuhiro Nagoya University, School of Medicine, Professor, 医学部, 教授 (50028669)
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| Co-Investigator(Kenkyū-buntansha) |
FUJIWARA Yoshihiro Nagoya University, School of Medicine, Research Associate, 医学部, 助手 (70238640)
ISHIKAWA Naohisa Aichi Medical College, Professor, 教授 (80109321)
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| Project Period (FY) |
1997 – 1999
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| Keywords | neurogenic pulmonary edema / lung / vascular permeability / central nervous system / pulmonary edema / neuropeptide Y / sympathetic nervous system / nitric oxide |
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| Research Abstract |
A variety of chemical mediators has been known to be responsible for the development of permeability pulmonary edema. We have been investigating the mechanisms of neurogenic pulmonary edema by using a rat model in which fibrinogen and thrombin are injected into the cisterna magna (neurogenic pulmonary edema model), and have found that neuropeptide Y (NPY) and neurokinin A, simultaneously released from the sympathetic nerve terminal, increase pulmonary vascular permeability. In terms of NPY, we reported a pioneer work in which NPY is proved to be one of the permeability substances by using an isolated perfused lung model and stimulating the sympathetic nerve. We also clarified that NPY administered intratracheally increases lung vascular permeability dose-despondently in the same model. In the following study, we have found that NPY is present both in the edema fluid and in alveolar macrophages and the concentration is 1000 times higher than that found in plasma by using an immunohistochemical method.
In the present study, we have meticulously studied the effect of nitric oxide (NO) on the development of pulmonary edema. The present results may suggest that the mechanism of neurogenic pulmonary edema is peripherally related to the release of chemical mediators such as NPY from the sympathetic nerve terminal, and centrally related to NO in the central nervous system. Also in a preliminary study of rats in which the vagus nerve was severed several days before, neurogenic pulmonary edema was completely avoided. Although the precise mechanism is still not clear, the development of neurogenic pulmonary edema may be closely related to the effects of NO in the central nervous system and NPY in the peripheral sympathetic nerve terminal.
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