1997 Fiscal Year Final Research Report Summary
Experimental Research on Revensibility of Noise Induced Hearing Impaivment
| Project/Area Number |
08672001
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Otorhinolaryngology
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| Research Institution | University of Occupational and Environmental Health |
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Principal Investigator |
YOSHIDA Masatumi University of Occupational and Environmental Health, Medical School, Otolaryngol Asociate Professor, 医学部, 助教授 (00182783)
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| Project Period (FY) |
1996 – 1997
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| Keywords | Noise exposure / solicylate / 2f_1-f_2 distortion product / Cochleon microphoncas / Otoacoustic emission / Electrical Stimuletion / Hearing impariment / outer hair cell |
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| Research Abstract |
Results and conclusions of the researches during the period from 1996 to 97 were as follows.
1. Suppression of the 2f1-f2 distortion product (DP) by the third tone was measured in cochlear microphonics (CM) and otoacoustic emissions (OAE). The suppression properties in the CM-DP and the DPOAE were similar to each other. This indicated that the both DP have a common generation mechanisms, and that the data on the CM-DP obtained from our animal experiments on acoustic overstimulation can be applied aptly to the DPOAE in daily clinic.
2. Acoustic responses were evoked by direct electrical simulation to the cochlea using a constant alternating current stimulator made in our laboratory. Measurement of the acoustic responses, electrically evoked otoacoustic emissions (EEOAEs) , in which stable responses could be obtained with simple and easy preparation, was considered a potential procedure for assessing the electro-mechanical transduction of the outer hair cells in vivo.
3. The EEOAEs were measured after acoustic overstimulation or administration of salicylate, both of which produced temporary threshold elevation of the compound action potential in similar magnitude to each other. The output of EEOAE was reduced by around 12dB after salicylate administration, although acoustic overstimulation resulted in little diminution in the EEOAE output. These data suggested that the temporary threshold elevations in hearing were caused by suppression of the electro-mechanical transduction of the outer hair cells in salicylate administration and of the mechano-electrical transduction in acoustic overstimulation.
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