An experimental model of cochlear ischemia using the photosensitization reaction of rose bengal (RB) is reported. Ischemia was induced by the systemic administration of RB solution and localized irradiation of the cochlea with a green light of specific wavelength for RB activation. After the RB solution was administered, the cochlear blood flow was temporarily increased and then decreased, and the latency of wave I of the auditory brainstem response increased and the amplitude of wave I decreased after RB injection and finally wave I disappeared completely. A histological study revealed thrombus formation in the vessels of the irradiated cochlea not only in the stria vascularis and the spiral ligament, but also in the modiolus. L-Histidine, a scavenger of singlet oxygen (1O2) and hydroxyl radical (·OH), significantly prolonged cochlear dysfunction, but D-mannitol, a specific scavenger of ·OH did not, suggesting that 1O2 has an important role in this reaction.
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