Vulnerability of the gerbil cochlea to sound exposure during reversible ischemia

Hear Res. 1999 Oct;136(1-2):65-74. doi: 10.1016/s0378-5955(99)00109-4.

Abstract

Cochlear ischemia induces a sensorineural hearing loss, in part through a fast functional impairment of outer hair cellls. Assuming that the cochlea is rendered fragile during ischemia and reperfusion and that stimulation itself can jeopardize its functional recovery, we used a model of reversible selective cochlear ischemia in Mongolian gerbils to establish what type of sound exposure can be deleterious during and immediately after reversible ischemia. Several groups of gerbils were used, with different ischemia durations and levels of sound exposure. Control groups were only exposed to tones at 80 and 90 dB SPL during 30 min, while other groups underwent complete and fully reversible blockage of the labyrinthine artery, during 5.5 or 8 min, and were exposed to 60 or 80 dB SPL tones during 30 min. The amount of ischemia and reperfusion was measured by means of laser Doppler velocimetry, whereas outer hair cells' function was continuously monitored through distortion-product otoacoustic emissions (DPOAEs). The losses of DPOAE levels after 8 min transient ischemia and 60 dB SPL exposure were as large as those induced by 80 dB SPL exposures combined with 5.5 min ischemia, or 90 dB SPL exposures without ischemia, with a maximum loss around 25-30 dB, half an octave above the stimulus frequency. These results give evidence for an extremely high cochlear vulnerability to low-level sound exposure when associated with reversible ischemia. This vulnerability may have important clinical consequences in patients with cochlear circulatory disturbances.

MeSH terms

  • Animals
  • Cochlea / blood supply*
  • Cochlea / physiopathology*
  • Disease Susceptibility
  • Female
  • Gerbillinae / physiology*
  • Hair Cells, Auditory, Outer / physiology
  • Hearing Loss, Noise-Induced / physiopathology
  • Ischemia / physiopathology*
  • Laser-Doppler Flowmetry
  • Otoacoustic Emissions, Spontaneous
  • Reperfusion Injury / physiopathology*
  • Sound*
  • Time Factors