Effects of experimental cochlear thrombosis on oxygenation and auditory function of the inner ear.

Abstract

To elucidate the etiology and pathogenesis of sudden hearing loss, the effect of experimental cochlear thrombosis on oxygenation and the auditory function of the inner ear was investigated in anesthetized guinea pigs. Impairment of cochlear blood flow (CBF) was induced by ferromagnetic obstruction of cochlear blood vessels at lowered body temperature. Perilymphatic oxygen partial pressure (PO2) in the basal scala tympani (about 200 microm below the round window membrane) was measured polarographically using micro-coaxial needle electrodes. Auditory function was examined by recording cochlear microphonic (CM) frequency responses, compound action potentials (CAP) and auditory evoked brainstem responses (ABR). Findings demonstrated a considerable decrease in the mean perilymphatic PO2 of 40%, 2 h after the start of the experiment. Mean CM and N1 CAP amplitudes were reduced by about 25% each and ABR by 18%. No significant changes were observed in the latencies of either CAP or ABR. Mean basal CBF was found to decrease by 35%, as measured by laser Doppler flowmetry in a parallel study. The present findings demonstrate that vascular impairment in the inner ear results in a considerable drop in intracochlear oxygenation, causing a significant loss in the auditory response.