| Project/Area Number |
16591532
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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 | Nagoya University |
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Principal Investigator |
NISHIWAKI Kimitoshi Nagoya University, Graduate School of Medicine, Associate Professor (10189326)
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| Co-Investigator(Kenkyū-buntansha) |
ISHIKAWA Naohisa Aichi Medical University, School of Medicine, Professor (80109321)
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| Project Period (FY) |
2004 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2006: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2005: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2004: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | neurogenic pulmonary edema / pulmonary endothelial cell / pulmonary vascular permeability / cell culture / vagal nerve / anesthetic agent / 神経原生肺水腫 / 血管透過性亢進 / Dibutyryl cAMP / neuropeptide Y / 部分肺還流標本 / ARDS / ALI |
|---|
| Research Abstract |
1. Establishment of neurogenic pulmonary edema induced by fibrin and thrombin injection to the 4th ventricle in rabbit : It was difficult to establish such model and finally abandoned that project.
2. Establishment of partially circulated rabbit lung preparation : This experiment was also stopped, because neurogenic pulmonary edema model in rabbit was failed.
3. Establishment of monolayer cell culture of human pulmonary endothelial cells : establishments of monolayer cell culture were succeeded in not only human pulmonary endothelial cells but also human coronary arterial endothelial cells and human aortic endothelial cells.
4. We investigated the permeability of monolayer of human pulmonary endothelial cells, using monolayer permeability models of endothelial cells, where a double incubation chamber was used for measurement of FITC-labeled albumin transfer through the monolayer. Isoflurane increased the permeability, but sevoflurane and propofol did not. The permeability increase induced by isoflurane was reversed by H-9 (PKG inhibitor), DY9760e (calmodulin inhibitor) and ML-7 (MLCK inhibitor), meaning that isoflurane increased pulmonary endothelial monolayer permeability through cytoskeleton change mediated by cGMP dependent kinase and myosin contraction mediated by myosin light chain kinase.
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