Abstract
Animal models have contributed to our understanding of cochlear injuries. In this report, generation mechanisms of the cochlear ischemia-reperfusion injury were examined using animal models. Increase in the extracellular concentration of glutamate is one of key components in the sequence of the cochlear ischemia injury. In addition, enhanced generation of free radicals and nitric oxide following reperfusion contributed to the further injury of outer hair cells. The present findings are important in the light of an attenuation of the cochlear ischemia-reperfusion injury.
