Complex level alterations of the 2 f 1 − f 2 distortion product due to hypoxia in the guinea pig

It is controversially discussed inasmuch acute hearing disorders might originate from impaired cochlear circulation. Hypoxia-specific alterations of inner ear parameters measurable in patients with acute sensorineural hearing loss would therefore be of great interest. Aim of this study was to characterize hypoxia-related alterations of the 2 f 1 − f 2 distortion product. Nine guinea pigs were anaesthetized by i.m. administration of Midazolam, Medetomidin and Fentanyl. For introduction of hypoxia, the spontaneously breathing animals were offered a gas mixture of N 2 O and O 2 containing either 21 or 12–13% O 2 . Distortion product otoacoustic emissions (DPOAEs) were continuously monitored at f 2 = 16 kHz; f 2 / f 1 = 1, 2; DP-definition = 2 f 1 − f 2 ; L 1 = 65 dB and L 2 = 55 dB, while inhaled oxygen was switched from 21 to 12–13% and back. Oxygen saturation (SaO 2 ) was continuously monitored. Data from an hypoxic interval were only used for further data processing if DPOAE levels were stable before and after hypoxia. Six hypoxic intervals in five animals fulfilled the stability criterion. During the hypoxic interval with the highest measured SaO 2 (75%), no alterations of DPOAE levels were observed. During the remaining five hypoxic intervals, when SaO 2 ranged between 57 and 70%, DPOAE levels were on average lower with an increased standard deviation compared to mean pre-hypoxic levels. Mean decrease correlated with the decrease of SaO 2 ( r = 0.90, P = 0.014). Alterations followed a characteristic time course—when hypoxia was started, DPOAE levels exhibited a short increase before they decreased and remarkably destabilized. After re-oxygenation DPOAE levels showed a pronounced level decrease, while SaO 2 already had recovered to pre-hypoxic values. After reaching a minimum, DPOAE levels slowly recovered to pre-hypoxic values. The decrease of DPOAE levels during hypoxia and the post-hypoxic level alterations have similarly been described by other authors before, while the distinct destabilization and transiently increased DPOAE levels have not been explicitly mentioned. A micromechanical mechanism that might explain a transient level increase and the post-hypoxic DPOAE level changes is discussed.