A rabbit model was developed to simulate the effects of ischemia that may occur during surgical removal of tumors involving the cerebellopontine angle or internal auditory canal. Specifically, the internal auditory artery was visualized through a posterior craniotomy and mechanically compressed for repetitive 1-minute intervals with a micromanipulator-controlled glass pipet terminating in a smooth bead. The 2f1-f2 distortion-product otoacoustic emissions were used to monitor the susceptibility of cochlear function to compressive effects. Distortion-product otoacoustic emissions were measured during discrete preblock, block, and postblock periods to determine the time course of distortion-product otoacoustic emission reduction and its return to baseline levels after rapid obstruction and resumption, respectively, of the cochlear vascular supply. Comparisons during these times indicated that preblock distortion-product otoacoustic emission levels were very stable, often varying by less than 1 dB. Additionally, distortion-product otoacoustic emissions were very sensitive to brief vascular occlusions in that, within approximately 25 seconds of blockage onset, emission levels at all frequencies decreased at rates of about -1.5 dB/second. On alleviation of the occlusion, distortion-product otoacoustic emissions rapidly and completely returned to preblock levels with a delay of about 4 seconds and recovery slopes of about 10.5 dB/second. A notable finding in some animals was that early and reproducible variations in distortion-product otoacoustic emission levels occurred within 5 to 8 seconds of internal auditory artery compression. When present, these transitory changes in distortion-product otoacoustic emission levels acted as early warning signs for vascular compromise of cochlear function.
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