초록 열기/닫기 버튼
Background and Objectives：In neonatal hyperbilirubinemia, accumulation of unconjugated bilirubin in the central auditorypathway and basal ganglia may cause sensorineural hearing loss and neurologic sequelae. The effect of unconjugated bilirubinon the brain is known well through auditory brainstem responses (ABRs). However, there is no evidence of pathologic changesin the cochlea. Jaundiced (jj) Gunn rats have been used as a good animal model for hyperbilirubinemia-related auditory dysfunction.The purpose of this study is to evaluate the bilirubin ototoxicity using ABR and DPOAE in jaundiced Gunn rats beforeand after sulfadimethoxine injection. Materials and Method：Experiments were conducted on three homozygous (jj) P19(postnatal 19 days) littermates, one heterozygous Gunn rat, five P21 jj littermates, and one nj Gunn rat littermate. P21 jj and njGunn rats were re-tested in three weeks in the same condition. ABR with 100-microsecond pulse width click and DPOAEs at8 kHz, 16 kHz and 22 kHz were measured before and after 1 mg/kg sulfadimethoxine injection. Results：The thresholds ofABR were elevated in P19 and P21 group within the first day after injection and became normalized at several days afterinjection. Delay of wave II, III, IV and V were also observed. DPOAE showed no significant change after injection in all groups,meaning that the cochlea was not damaged. Conclusion：This study shows that bilirubin ototoxicity is related with pathologicchanges at or higher than the brainstem level with intact cochlear function. Changes in ABR findings were only observed in P19and P21 groups because they had higher bilirubin level in blood and their central auditory pathway is more immature than thatfound in the P42 group. In this study, we also found the possibility of spontaneous recovery from hyperbilirubinemia-relatedauditory toxicity.
키워드열기/닫기 버튼
Gunn Rats·Hyperbilirubinemia·Auditory brainstem response·Spontaneous otoacoustic emission.
