Aim:To investigate the changes of neuronal nitric oxide synthase (nNOS) activity in the cochlear nuclei and auditory brainstem response (ABR) during brainstem ischemia.Methods:A total of 55 guinea pigs were randomly a...Aim:To investigate the changes of neuronal nitric oxide synthase (nNOS) activity in the cochlear nuclei and auditory brainstem response (ABR) during brainstem ischemia.Methods:A total of 55 guinea pigs were randomly allocated into five groups:normal control group, sham operation group, ischemia group,7-NI group, and vehicle group. The animal models of vertebrobasilar ischemia were prepared by unilateral carotid clamping as well as basilar artery occlusion. 7-Nitroindazole (7-NI), a selective inhibitor of nNOS, was administered intraperitoneally 5 minutes before the onset of ischemia. Results: Changes of ABR in the vertebrobasilar ischemia condition consisted of a delay in all wave latencies and an increase of the auditory threshold. The nNOS activity in the cochlear nuclei increased significantly as early as 15 min, peaked at 30 min, and returned to basal level at 60 min after ischemia. The wave latencies, interpeak latencies, and thresholds of ABR decreased in T-NI group compared with those in ischemia group (P<0.05). Conclusions:nNOS is involved in early cochlear nuclei ischemia injury. nNOS selective inhibitor 7-NI, as a potential therapeutic agent in neuron ischemia can protect the auditory function against excessive production of NO.展开更多
文摘Aim:To investigate the changes of neuronal nitric oxide synthase (nNOS) activity in the cochlear nuclei and auditory brainstem response (ABR) during brainstem ischemia.Methods:A total of 55 guinea pigs were randomly allocated into five groups:normal control group, sham operation group, ischemia group,7-NI group, and vehicle group. The animal models of vertebrobasilar ischemia were prepared by unilateral carotid clamping as well as basilar artery occlusion. 7-Nitroindazole (7-NI), a selective inhibitor of nNOS, was administered intraperitoneally 5 minutes before the onset of ischemia. Results: Changes of ABR in the vertebrobasilar ischemia condition consisted of a delay in all wave latencies and an increase of the auditory threshold. The nNOS activity in the cochlear nuclei increased significantly as early as 15 min, peaked at 30 min, and returned to basal level at 60 min after ischemia. The wave latencies, interpeak latencies, and thresholds of ABR decreased in T-NI group compared with those in ischemia group (P<0.05). Conclusions:nNOS is involved in early cochlear nuclei ischemia injury. nNOS selective inhibitor 7-NI, as a potential therapeutic agent in neuron ischemia can protect the auditory function against excessive production of NO.
