Measurement of DPOAE after ischemia/reperfusion injury of the cochlea in gerbils.
The effects on distortion product otoacoustic emissions (DPOAEs) during the late phase of ischemia/reperfusion injury in the cochlea were studied. Ischemia/reperfusion injury was induced in a gerbil model by occluding both vertebral arteries for 15min. Hearing was assessed by recording compound action potentials (CAPs) before, during, and 7 days after ischemia. The histological changes in the hair cells were evaluated in specimens stained with rhodamine-phalloidin and Hoechst 33342. The average increase in CAP threshold 7 days after ischemia was 16.3+/-8.0dB at 8kHz. In contrast, interruption of the blood supply to the cochlea decreased the DPOAE amplitudes to the noise floor; this usually recovered to the same level as that seen under pre-ischemic conditions 7 days after ischemia. Histologically, the mean respective losses of inner and outer hair cells (IHCs and OHCs, respectively) of the inner ear were 26.5% and 3.3% in the basal turn, respectively. These results indicate that in gerbils OHCs are tolerant to ischemia/reperfusion injury pathologically and physiologically because DPOAE is closely related to the active process of OHCs and is a useful test to examine OHC function.
Watanabe
Futoshi
F
Department of Otolaryngology, Ehime University School of Medicine, Shigenobu-cho, Toon city, Ehime 791-0295, Japan.
Hakuba
Nobuhiro
N
Gyo
Kiyofumi
K
D000200:Action Potentials; D000818:Animals; D003051:Cochlea / Q000098:blood supply / Q000473:pathology / Q000503:physiopathology*; D005849:Gerbillinae; D006199:Hair Cells, Auditory, Inner / Q000473:pathology; D018072:Hair Cells, Auditory, Outer / Q000473:pathology; D017084:Otoacoustic Emissions, Spontaneous; D015427:Reperfusion Injury / Q000473:pathology / Q000503:physiopathology*