The purpose of the present study was to further elucidate how nitric oxide (NO) is involved in cochlear anoxia-reperfusion injury. Transient local anoxia of the cochlea was induced in albino guinea pigs for 15, 30, or 60 minutes by transiently compressing the labyrinthine artery through a skull base approach. 7-Nitroindazole (7NI), a relatively selective neuronal nitric oxide synthase (nNOS) inhibitor. was intraperitoneally administered to the guinea pigs 30 minutes before the onset of local anoxia. The compound action potential (CAP) thresholds were measured before the administration of 7NI and 4 hours after the onset of reperfusion. A statistically significant reduction in the postanoxic CAP threshold shift from the preadministration value was observed in the 7NI-administered animals as compared with the control animals after 15- and 30-minute periods of anoxia. These results confirm the involvement of NO and nNOS in the cochlear injury induced by transient local anoxia.