摘要
Objectics: To demonstrate the effects of NO synthase (NOS ) blockade on the OHCs. Methods: The Nnitro L-arginine (L-NNA) was used and the vibration velocity of basilar membrane (BMV ) was observed. Pigmented guinea pigs were anesthetized and surgically prepared to permit infusion of L- NNA into the scala tympani of basal turn of cochlea . The basilar membrane (BM ) vibration and compound action potential (cAP ), endocochlear potential (EP ) and cochlear mierophonic (CM ) were monitored. Eight μ1 of 1. 6 mmol/L- L- NNA was infused into the perilymph of scala tympani . The BM velocity responses elicited with direct current (DC ) pulses were recorded. Results: The BMV was increased by approximately 3 folds following infusion of L-NNA. The CM de creased by a small amount and there was no significant change in CP. This phenomenon occurs only in the cochlearsensitivity has been lost less than 40 dB . No improvement in BM velocity if the cochlear sensitivity was ’normal’ or was damaged too severely. Conclusion: The results imply that NO bas the excitotoxicity on OHCs, it can promote the injury of cochlea when noise is exposed. L-NNA may act as a guardian when facts of trauma act on cochlea.
Objectics: To demonstrate the effects of NO synthase (NOS ) blockade on the OHCs. Methods: The Nnitro L-arginine (L-NNA) was used and the vibration velocity of basilar membrane (BMV ) was observed. Pigmented guinea pigs were anesthetized and surgically prepared to permit infusion of L- NNA into the scala tympani of basal turn of cochlea . The basilar membrane (BM ) vibration and compound action potential (cAP ), endocochlear potential (EP ) and cochlear mierophonic (CM ) were monitored. Eight μ1 of 1. 6 mmol/L- L- NNA was infused into the perilymph of scala tympani . The BM velocity responses elicited with direct current (DC ) pulses were recorded. Results: The BMV was increased by approximately 3 folds following infusion of L-NNA. The CM de creased by a small amount and there was no significant change in CP. This phenomenon occurs only in the cochlearsensitivity has been lost less than 40 dB . No improvement in BM velocity if the cochlear sensitivity was 'normal' or was damaged too severely. Conclusion: The results imply that NO bas the excitotoxicity on OHCs, it can promote the injury of cochlea when noise is exposed. L-NNA may act as a guardian when facts of trauma act on cochlea.
