Protection of outer hair cells from reperfusion injury by an iron chelatorand a nitric oxide synthase inhibitor in the guinea pig cochlea

To examine whether an active process of the cochlea was injured by ischemia -reperfusion, time courses of distortion-product otoacoustic emissions (DPO AEs) were examined before, during and after 30 min cochlear ischemia using albino guinea pigs. DPOAEs decreased to the minimum level when the animals were subjected to ischemia. When the cochlea was recirculated, DPOAEs initi ally recovered with time until 20 min after the onset of reperfusion. Howev er, thereafter the amplitude of DPOAEs gradually decreased toward the noise level. Administration of deferoxamine (an iron chelator) or N-nitro-L-argi nine (a nitric oxide synthase inhibitor) ameliorated this decrease of DPOAE s during reperfusion and significantly increased the DPOAE amplitudes 60 mi n after the onset of reperfusion as compared with those in non-treated anim als. These results suggest that cochlear reperfusion as well as ischemia in jured the active process of the cochlea and that free radicals and nitric o xide play important roles in this injury. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.