[Effects of salicylate on electrically evoked otoacoustic emissions in the guinea pig].

Clinically, salicylates have been known to have a ototoxic side effect of reversible hearing loss and to reduce the voltage-dependent length change (electromotility) in experiments on isolated outer hair cells (OHC). In order to clarify how the reduction of OHC electromotility due to salicylates contributes to cochlear dysfunction in vivo, we observed compound action potentials (CAP) threshold as well as the outputs of the electrically evoked otoacoustic emissions (EEOAE) before and after intravenous administration of 500 mg/kg sodium salicylate in a guinea pig model. A silver ball electrode placed on the round window membrane of the animal was used for both recording of the CAP and stimulation to elicit the EEOAE. The CAP threshold to tone bursts with frequencies from 2 to 10 kHz elevated by 13 to 22 dB, and outputs of the EEOAE decreased approximately 4 dB for 5 kHz stimulation, and 12 dB for 8 kHz after salicylate administration. These results suggested that systemically administered salicylate also reduced the electromotility of the OHC, and caused the hearing impairment in vivo.