Contribution of the Ischemic-Reperfusion Mechanism to Nasal Hyper Sensitivity
| Project/Area Number |
06671740
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Otorhinolaryngology
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| Research Institution | Kansai Medical University |
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Principal Investigator |
KUBO Nobuo Kansai Medical University, Associate Professor, 医学部, 助教授 (70186435)
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| Co-Investigator(Kenkyū-buntansha) |
NAKAMURA Akihiko Kansai Medical University, Assistant Professor, 医学部, 講師 (90180356)
KITAJILI Masanori Kansai Medical University, Associate Professor, 医学部, 助教授 (60161478)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1995: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1994: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | Endothelial Cells / Nasal Mucosal / Histamine / NO / Intracellular Ca^2+ Concentration / ATP / Nasal allergy / 鼻過敏症 / 鼻茸症 / 活性酸素 / 一酸化窒素 / 虚血-再環流障害 |
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| Research Abstract |
We have investigated chronic inflammatory symptoms of perennial nasal allergy, such as nasal blockage and nonspecific hypersensitivity. We have verified the edematous swelling of turbinate mucosa which is found in most of perennial allergy is related to ischemic event of nasal microvascular circulation, not likely to the congestion of turbinate mucosa of patient with seasonal nasal allergy. Our recent hypothesis of above mechanism is that functional disturbance of NO production of vascular endothelial cells and the ischemic reperfusion phenomenon of epithelial cells might contribute mucosal edema of turbinate in cases with perennial nasal allergy.
In this project, we verified a couple of evidences of above mechanism. 1) Intracellular Ca Mobilization in cultured Human Mucosal Microvascular Endothelial Cells from Nasal Inferior turbinate. 2)Histamine-induced Ca released from cultured human mucosal microvascular endothelial cells from nasal inferior turbinate.
Inflammatory mediators affect microvascular endothelial cells, relating dysfunction of NO production, which is one of the aspect of the pathophysiology of chronic nasal allergy.
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Report
(3 results)
Research Products
(8 results)
