• Nevreste Didem Sonbay Yilmaz, Cem Saka, Sibel Alicura Tokgöz, Murat Çalişkan, Erkan Vuralkan, and Ömer Beşalti.
• Department of Ear, Nose, and Throat, Antalya Education and Training Hospital, Antalya, Turkey
• Turk J Med Sci. 2020 Oct 22; 50 (6): 1580-1584.

Background/AimIschemia is insufficient blood flow to provide adequate oxygenation. In the present study, we aimed to show whether acute hypoxia has a critical oxygen value that may lead to the deterioration of cochlear function.Materials And MethodsUnder general anesthesia, prehypoxic signal-to-noise ratios were determined by distortion product otoacoustic emissions (DPOAE). The oxygen saturation (SaO2) values of rats were monitored with an oxygen saturation probe. Rats were injected with an extra dose of anesthetic agent, and SaO2 was reduced. DPOAE values in SaO2 100–90, 90–80, 80–70, and 70–60 posthypoxic values were measured and compared statistically with prehypoxic values.ResultsAt 3000 and 4000 Hz, SaO2 70–60 values measured after the hypoxia were observed to be statistically significantly lower than the values measured before the hypoxia. At 6000 and 8000 Hz, SaO2 80–70 and 70–60 values measured after the hypoxia were observed to be statistically significantly lower than the values measured before the hypoxia. At 10,000 Hz, all of the values measured after the hypoxia were observed to be statistically significantly lower than the values obtained before the hypoxia.ConclusionMany studies have been conducted on the effects of hypoxia on the inner ear. It remains unclear how fluctuations in DPOAE levels affect hearing in clinical trials when the SaO2 starts to decrease. Although hypoxia has been implicated in the etiology of sudden hearing loss and tinnitus, the effects of acute hypoxia on the cochlea are still uncertain. Further studies are needed on this subject.This work is licensed under a Creative Commons Attribution 4.0 International License.

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