Project/Area Number |
04671057
|
Research Category |
Grant-in-Aid for General Scientific Research (C)
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Allocation Type | Single-year Grants |
Research Field |
Otorhinolaryngology
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Research Institution | KANSAI MEDICAL UNIVERSITY |
Principal Investigator |
TOMODA Koichi KANSAI MEDICAL UNIVERSITY,ASSOCIATE PROFESSOR, 医学部, 助教授 (50164041)
|
Co-Investigator(Kenkyū-buntansha) |
KUBO Nobuo KANSAI MEDICAL UNIVERSITY ASSISTANT PROFESSOR, 医学部, 講師 (70186435)
|
Project Period (FY) |
1992 – 1993
|
Project Status |
Completed (Fiscal Year 1993)
|
Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1993: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1992: ¥1,500,000 (Direct Cost: ¥1,500,000)
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Keywords | Meniere's disease / Endolymphatic hydrops / Endolymphatic sac / Immunopathology / Inner ear biology / Perilymphatic fistula / 免疫学 / メニエール氏病 / 内リンパ管破壊 / 自己免疫病 / 対宿主移植片病 / 骨髄移植 |
Research Abstract |
We have investigated the immunological role of endolymphatic sac in the occurrence of endolymphatic hydrops which is the main pathology of Meniere's disease. On the study of functional and immunopathological alterations after interruption of endolymphatic duct, Na^+ and K^+ concentration and DC potential in the sac showed significant reduction. The amount of stainable substance in the sac lumen was increased for a few week. These findings suggested that an active transport and/or passive diffusion of ions across sac epithelium would be disturbed in the interrupted sac, and the stainable substance increased may play an important role in the regulation of pressure/volume homeostasis in the endolymphatic system. Immunopathological study using sensitized guinea pigs which were already interrupted endolymphatic duct revealed that after secondary immunization of KLH or HRP into the sac, there were no significant increase of antibodies in the perilymph. While in the animals which were not int
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errupted duct, the perilymphatic antibody levels were significantly increased following same secondary immunization. This finding suggests that the endolymphatic sac is an important site in the inner ear immune response. Furthermore, using graft versus host disease model after bone marrow transplantation, the immunocompetent cells distributed in the endolymphatic sac may be derived from systemic circulation. On the other hand, it has been reported that the endolymphatic hydrops appear to be due to the secondary injury of perilymphatic fistula. We have investigated the temporal bone pathology of the guinea pigs with experimentally induced perilymphatic fistula. In the early stage of experiment, the cochlea showed hydrops due to the rapid reduction of perilymphatic pressure while the vestibule showed collapse due to the damage of trabecular mesh. In the late stage (2 weeks) of experiment, the vestibule showed hydrops in association with the obliteration of utricular-fold. This model suggests that the structural abnormality induced by the perilymphatic fistula may produce secondary hydrops and may possibly be one of etiology of Meniere's disease. Less
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