Experimental Studies on the Mechanism and Promoter of Acoustic Hearing Impairment.

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The mechanism and promoter of noise-induced hearing impairment have been investigated in the animal study using guinea pigs. Obtained results were as follows :1. The CAP thresholds of the animals exposed to 4kHz pure tone at 120 dB for 10 minutes elevated by 60 dB right after the exposure, and then recovered to reach the permanent threshold shift of 30 dB at 7 days after. The electrically evoked otoacoustic emissions (EEOAEs) did not reveal any alteration at the period both right after and 7 days after the exposure. From these result it was concluded that dysfunction of the mechano-electrical transduction (MET) of the outer hair cells was responsible for the noise-induced temporary as well as permanent threshold shift.2. Glucocorticoid (GR) receptor antagonist, RU38463, was administered to the animals at 0, 3 and 7 days after the exposure to 4 kHz pure tone at 120 dB SPL for 10 minutes. The CAP threshold elevation in these animals were significantly sever at the frequencies from 5 to 8 kHz as compared to the saline injected annuals at 7 days after the exposure. Down regulation of GR-GR receptor system in the cochlea affected the recovery fiom noise-induced temporary threshold sift, and thus accelerate the susceptibility to acoustic overstimulation.3. Acoustic modulations of 12 kHz EEOAEs by low frequency tone were measured before and after the exposure to 8 kHz band noise at 103 dB SPL for 30 minutes. The output of the EEOAEs itself was not affected by the exposure, but the magnitudes of acoustic modulation were decreased by 50 %. Loss of the MET function due to loud sound exposure was considered to reduce the magnitude of acoustic modulation in EEOAEs.