Clarification of the pathophysiology of brain death-associated lung function impairment and research on the precaution and remedy
| Project/Area Number |
23592251
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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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 |
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| Co-Investigator(Renkei-kenkyūsha) |
ISHIKAWA Naohisa 愛知医科大学, 医学部, 教授 (80109321)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 神経原性肺水腫 / 細胞透過性 / 肺動脈内皮細胞 / 神経ペプチドＹ / 麻酔薬 / 脳死肺移植 / 肺動脈血管内皮細胞 / 神経ペプチドY / 脳死 / 肺移植 / 神経原生肺水腫 / ARDS / 肺血管透過性 / neuropeptide Y / ＡＲＤＳ |
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| Research Abstract |
It has been suggested as a reason for the difficulty in the lung transplantation from a brain-dead donor that brain edema and increased intracranial pressure induce neurogenic pulmonary edema (NPE) resulting in the lung function impairment. In the present study, we established an in vitro human pulmonary endothelial cell model and assessed the effect of neuropeptide Y (NPY), which was discovered as a causative agent in NPE, on cell permeability. NPY alone showed no statistically significant enhancement of cell permeability in the range from 1 x 10-11 to 1 x 10-7 M. In addition, neither hypoxic (5% O2) condition nor combination with norepinephrine caused NPY-induced cell permeability. These results suggest that the site of action of NPY is not in pulmonary endothelial cells in NPE.
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Report
(4 results)
Research Products
(19 results)
