Noise-Induced Cochlear Hypoxia Is Intensity Dependent, Correlates with Hearing Loss and Precedes Reduction of Cochlear Blood Flow

Abstract

Anesthetized and artificially ventilated guinea pigs were exposed to broad-band noise of 95, 101, 106 or 115 dB SPL for 30 min and studied for 180 min after cessation of noise. The partial pressure of oxygen (pO₂) in the perilymph, the cochlear blood flow (CoBF) and auditory-evoked potentials were continuously recorded. Arterial blood pressure, electrocardiogram, inspiratory and expiratory gas levels, arterial blood gas levels and acid-base status were kept stable to exclude influences of these parameters on cochlear parameters. Exposure to 95 dB SPL did not affect perilymphatic pO₂or CoBF. Cochlear microphonics (CMs) were reduced, but compound action potentials of the auditory nerve (CAPs) and auditory brainstem potentials (ABRs) increased after exposure to this low-level noise. Perilymphatic pO₂decreased during exposure to 101 dB SPL and then further decreased during the subsequent 60 min after cessation of the noise. CoBF did not change significantly during and 30 min after noise but then paralleled the decline of perilymphatic pO₂ However, both parameters showed a clear indication of recovery in the sec-ond and third hours after noise. At 101 dB SPL, CMs were again reduced immediately, CAPs were unaltered and ABRs again increased. Exposure to 106 and to 115 dB SPL resulted in a decrease in both perilymphatic pO₂and CoBF; this decrease began during the exposure but became progressively worse after the noise. Hearing loss was observed immediately with exposure and showed no signs of further deterioration after cessation. The observed time courses of changes are important. They reveal that hearing loss and cochlear hypoxia precede reduction in CoBF due to noise exposure. The potential mechanisms underlying these effects are discussed.

Cochlear Pericyte Responses to Acoustic Trauma and the Involvement of Hypoxia-Inducible Factor-1α and Vascular Endothelial Growth Factor

“…26,27 The hypoxic environment induced in the cochlea by noise is immediate and the effects persist after the noise is terminated. 6,28 Studies have shown that when cells encounter low oxygen tension, they adapt by promoting expression of genes associated with anaerobic cell metabolism, cell survival, and angiogenesis. 29 This transcriptional response is mediated by a hypoxia-induc-ible factor (HIF), 30,31 a principal transcription factor, involved in the regulation of transcriptional responses to hypoxia.…”

Morphological and Functional Positive Effect with the Association of Hyperbaric Oxygen Therapy and Corticoid Against Acute Acoustic Trauma

“…Changes in oxygenation and decreased cochlear blood flow appear to occur first, inducing an accumulation of free radicals in the cochlea that triggers proce and cell death [12][13][14][15].…”

Noise exposure during ambulance flightsand repatriation operations

“…Since the auditory hair cells get their oxygen by diffusion, the hypobaric hypoxia present in the cabin of an aircraft during a flight -which typically provides an equivalent pressure of about 2000 to 2300 m -may increase the risk of hearing loss due to noise. The additional risk of hypoxia may contribute to a reduced cochlear capillary perfusion and result in the decrease of perilymphatic oxygen partial pressure induced by the noise [17,18]. Both these effects risk factor for hearing loss.…”