Abstract
Possible otoprotective properties of cocarboxylase were studied on the model of amikacin-induced ototoxicity in immature rabbits. Auditory function was evaluated by the short-latency auditory brainstem response (ABR) and distortion product otoacoustic emission (DPOAE) tests. Administration of cocarboxylase after modeling of amikacin-induced ototoxicity resulted in a decrease in the ABR peak I threshold and prevented damage to the outer hair cells.
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