| Project/Area Number |
63570816
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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 | Osaka City University |
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Principal Investigator |
NAKAI Yoshiaki Osaka City University Medical School, Professor, 医学部, 教授 (10046998)
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| Co-Investigator(Kenkyū-buntansha) |
MASUTANI Haruhiko Osaka City University Medical School, Assistant, 医学部・耳鼻咽喉科, 助手 (10190357)
KONISHI Kazuo Osaka City University Medical School, Assistant, 医学部・耳鼻咽喉科, 助手 (50145801)
OHASHI Yoshihiro Osaka City University Medical School, Instructor, 医学部・耳鼻咽喉科, 講師 (60160602)
YAMANE Hideo Osaka City University Medical School, Instructor, 医学部・耳鼻咽喉科, 講師 (60145787)
CHO Hiromasa Osaka City University Medical School, Associate Professor, 医学部・耳鼻咽喉科, 助教授 (60128741)
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| Project Period (FY) |
1988 – 1990
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| Project Status |
Completed (Fiscal Year 1990)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1990: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1989: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1988: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | Sound Exposure / Cochlear Blood Flow / EndolYmphatic Hydrops / Hair Cell / Evoked Otoacoustic Emission / 内耳傷害 / 細胞培養 / 強大音 / 感音難聴 / 内耳血管 / 血流 / 走査 / 透過電子顕微鏡 |
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| Research Abstract |
Blood circulation in the cochlea after exposure to a non-physiological level of sound (100-125 dB SPL, 3h) was investigated by immunohistological methods and blood vessel casting method by SEM. Impaired blood circulation in the capillary of stria vascularis, osseous spiral lamina and spiral prominence, especially strial capillary showed vasoconstriction like change from early time of this sound exposure and its recovery to the normal status needed more than 24 hours. On the other hand, these capillaries showed no remarkable change after relatively physiological sound level (70-80 dB SPL, 20 min) exposure. These data suggest that NITTS (Noise-induced Temporary Threshold Shift) is ascribed to blood circulation impairment in these areas of the cochlea.
In the case of endolymphatic hydrops which is the pathological change manifested in the inner ear dysfunction, the acoustic trauma combined, much more damage was recognized in the hair cell in the cochlea. Glycerol administration might slightly decrease this damage.
The normal hearing ear was not affected in the shape of evoked Oto Acoustic Emission (e-OAE) by the difference of time duration of 1 K Hz tone burst stimulation. The ear which had endolymphatic hydrops showed lower tone frequency of e-OAE than stimulated frequency. The administration of lidocaine hydrochloride and loop diuretics showed the change of e-OAE curve.
Our devised LV therapy was adopted to the treatment of the patients with acoustic trauma and its usefullness was statistically recognized.
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