1990 Fiscal Year Final Research Report Summary
The Mechanism of Hearing Loss Due to Acoustic Trauma
| 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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| Keywords | Sound Exposure / Cochlear Blood Flow / EndolYmphatic Hydrops / Hair Cell / Evoked Otoacoustic Emission |
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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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[Publications] Hachikawa, K, Yamane, H., Kato, S., Kato, M., Aiba, T., Matsuda, Y. and Nakai, Y.: "Middle ear disease and endolymphatic hydrops." Equilibrium Res. Suppl. 4. 104-108 (1988)
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[Publications] Konishi, K, Yamane, H., Hachikawa, K., Sakamoto, H., Matsuda, Y. and Nakai, Y.: "Distribution of kanamaycin sulfate in the peripheral vestibular organ." Equilibrium Res. Suppl. 5. 54-58 (1989)
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[Publications] Matsunaga, K., Nakai, Y., Masutani, H., Sugita, M., Moriguchi, M. and Okamoto, J.: "Observation of inner ear vessels in experimental hydrops." Equilibrium Res. Suppl. 5. 112-115 (1989)
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[Publications] Masutani, H., Nakai, Y., Sugita, M., Moriguchi, M., Matsunaga, K. and Okamoto, J.: "The influence of noise exposure on experimental hydrops in the guinea pig." Equilibrium Res. Suppl. 6. 36-39 (1990)
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[Publications] Yamane, H., Nakai, Y., Konishi, K., Sakamoto, H., Iguchi, H., Nakagawa, T., Morinaka, K. and Takahashi, K.: "Inner ear hair cell mobility and cytoskeleton." Equilibrium Res. Suppl. 6. 47-51 (1990)
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