Effect of hypoxemia and ethacrynic acid on ABR and distortion product emission thresholds

Sharon Freeman, Kalman Goitein, Joseph Attias, Miriam Furst, Haim Sohmer

Research output: Contribution to journalArticlepeer-review

Abstract

Various studies have shown that induction of hypoxemia in animals such that arterial blood oxygen tensions reach 20-30 mm Hg is accompanied by reversible threshold elevations of the auditory nerve-brain-stem evoked response (ABR). In this state, the endocochlear potential (EP) is depressed, causing a smaller potential difference across the hair cells and/or reduced activity of the cochlear amplifier of the outer hair cells. In order to test these possibilities, ABR threshold (an expression of the overall sensitivity of the cochlea) and changes in threshold of the cubic (2f1 - f2) distortion product emissions (DPE) (an expression of activity of the cochlear amplifier) were measured in the same cats while the EP was depressed by hypoxemia or by ethacrynic acid. During the episodes of hypoxemia, DPE thresholds were elevated by 10 dB while ABR thresholds were elevated by 22.8 dB. Therefore, it seems that a normal EP is necessary both for normal cochlear transduction (inner hair cells) and for normal cochlear amplification (outer hair cells). The human fetus in utero is relatively hypoxic and there is evidence that its auditory threshold is also similarly elevated. Therefore the threshold elevation in the fetus in utero, estimated to be about 20 dB, is a consequence of both reduced transduction current through the inner hair cells (about 10 dB) and an additional 10 dB reduction in the activity of the cochlear amplifier of the outer hair cells.

Original languageEnglish
Pages (from-to)21-29
Number of pages9
JournalJournal of the Neurological Sciences
Volume131
Issue number1
DOIs
StatePublished - Jul 1995
Externally publishedYes

Keywords

  • ABR
  • Cochlear amplifier
  • Distortion products
  • Emission
  • Ethacrynic acid
  • Hypoxia
  • Threshold

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

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