| Project/Area Number |
04671054
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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 | Nippon Medical School |
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Principal Investigator |
TOMIYAMA Shunichi Nippon Medical School, Otolaryngology, Associate Professor, 医学部, 助教授 (00094665)
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| Co-Investigator(Kenkyū-buntansha) |
YAMANOBE Sigeharu Nippon Medical School, Otolaryngology, Assistant Professor, 医学部, 講師 (20210510)
AOKI Hideharu Nippon Medical School, Otolaryngology, Assistant Professor, 医学部, 講師 (80159293)
後藤 裕一 日本医科大学, 医学部, 助手
池園 哲朗 日本医科大学, 医学部, 助手
野中 学 日本医科大学, 医学部, 助手
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| Project Period (FY) |
1992 – 1993
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| Project Status |
Completed (Fiscal Year 1993)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1993: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1992: ¥900,000 (Direct Cost: ¥900,000)
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| Keywords | Inner ear / Endolymphatic sac / Immune response / Attack of vertigo / Endolymphatic hydrops / Sensory hearing loss / Caloric response / Radical oxygen / 〓〓難聴 / 内耳免疫 / 蝸電図 / 聴性脳幹反応 / 自発眼振 / 外リンパ抗体 |
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| Research Abstract |
This study investigated pathophysiology of inner ear immune-injury in the animal model. Guineapigs were systemically presensitized with keyhole limpet hemocyanin (KLH) and were directly challenged with KLH to the endolymphatic sac (ES). Endolymphatic hydrops (EH) appeared in the saccule and the basal turn as soon as 5 hours and rapidly developed within 2 days. After one week, EH gradually disappeared. However, after 9 weeks, EH reccurred in the saccule, basal and apical turn. Cellular reaction in the ES obviously ocurred from 5 hours and reached maximum at 12 hours. These cells were acute inflammatory cells. After one week, lymphocytes and plasma cells were prodominant and remained for more than 3 months. In the acute inflammatory phase, hemorrhage occasionally occured mainly in the perilymphatic region in which case degeneration of sensory cells often accompanied. Myeloperoxidase distributed in the ES, sensory hair cells, spiral ligament and stria vasularis as soon as 5 hours and reached maximum within one day. Irritative spontaneous nystagmus occurred nearly after 12 hours and paralytic nystagmus followed nearly for 48 hours. Elevation of hearing threshold as well as suppression of caloric response occurred after 2 days and thereafter recoverd in most animals. Elevation in perilymphatic anti-KLH antibody levels within one week correlated well to the severity of morphophsyiological damage of the inner ear. These results suggested that recurrent immune reaction in the ES may lead to cause attack of vertigo, similar to Meniere's disease.
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