1996 Fiscal Year Final Research Report Summary
Study on the Mechanism of Increased Vascular Permeability in Pulmonary Edema
| Project/Area Number |
06454443
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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, Anesthesiology, Professor, 医学部, 教授 (50028669)
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| Co-Investigator(Kenkyū-buntansha) |
ISHIKAWA Naohisa Aichi Prefectural Institute of Hygiene, Pharmacology, Head, 所長
NISHIWAKI Kimitoshi Nagoya University School of Medicine, Anesthesiology, Assistant Professor, 医学部, 講師 (10189326)
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| Project Period (FY) |
1994 – 1996
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| Keywords | pulmonary edema / neurogenic pulmonary edema / vascular permeability / neurotransmitter / ARDS / neuropeptide Y / peptide YY / pulmonary circulation |
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| Research Abstract |
We investigated the role of neurotransmitters on the mechanism of pulmonary vascular permeability, and the following results were obtained in terms of the role of neuropeptide Y (NPY), which co-exists with norepinephrine in the sympathetic nervous system, on the development of pulmonary edema.
1)We studied the effect of sympathetic nerve stimulation on lung vascular permeability on isolated perfused lung model. Electrical stimulation increased the lung weight, suggesting an increase in lung vascular permeability. The increase in lung weight occurred in the presence of norepinephrine blockers, suggesting the presence of vasoactive substances other than norepinephrine.
2)By using the isolated perfused lung model, NPY and neurokinin A (NKA) showed an increase in capillary permeability coefficient (Kfc), and calcitonin-gene related protein (CGRP) showed a decrease.
3)Lung vascular permeability can be elucidated by injecting carbon particlesinto the perfusate of the lung model and microscopically calculate the carbon particles present in the alveoli. Administration of NPY into the trachea caused a significant increase in the number of carbon particlesin the alveoli in a dose-dependent manner.
4)Pretreatment with NPY_<18-36>, which is a partial antagonist of NPY Y_3 receptor, elongated the time required for edema formation and reduced the protein concentration ratio of alveolar fluid to serum in the fibrin pulmonary edema model.
5)Pretreatment with NPY_<18-36> reduced the number of carbon particlesin the alveoli in the animals treated with NPY intratracheally.
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