椎基底动脉缺血／再灌注对豚鼠听功能和耳蜗形态学影响

目的 探讨椎基底动脉缺血／再灌注耳蜗损伤后耳蜗病理形态学和听功能改变。方法经颅底径路建立豚鼠椎基底动脉缺血／再灌注耳蜗损伤模型。68只豚鼠随机分成6组：正常组、缺血1h组、缺血再灌注组（按再灌注时间分12h、24h、48h．7d，4组）。各组动物分别于手术前和处死前行听性脑干反应（auditory brainstem response，ABR）测定，观察ABR各波潜伏期、Ⅰ-Ⅲ波间期和Ⅲ波阈值，部分动物观察了缺血时ABR变化。耳蜗组织切片HE染色技术观察组织细胞形态变化。结果血管阻断缺血时ABR表现波形不典型，重复性差，在缺血10～20min后波形逐渐稳定；缺血组与再灌注（12h、24h、48h、7d）各组ABR各波潜伏期和Ⅰ-Ⅲ波间期较正常组延长，Ⅲ波阈值升高，尤以再灌注24h变化最为显著，48h和7d后ABR阈值有所恢复，但不能恢复正常。耳蜗病理形态学改变发现缺血组毛细胞变形肿胀，再灌注（12h、24h、48h．7d）各组损伤进一步加重，再灌注24—48h损伤最重，可见明显外毛细胞缺损，螺旋神经元胞体和神经纤维较正常组减少，血管纹变薄，均以基底转为明显。结论豚鼠椎基底动脉缺血／再灌注时可致耳蜗损伤，表现为听功能和耳蜗组织形态学改变。

The changes of auditory function and histomorphology of the cochlea on the vertebrobasilar artery ischemia reperfusion in guinea pigs

To investigate the changes of auditory function and histomorphology of cochlea during the reperfusion of vertebrobasilar artery in guinea pigs.Methods Sixty-eight healthy guinea pigs with normal Preyer's reflex weighed from 200～250 g were used in this study. They were randomly divided into 6 groups: the normal control group、the ischemia 1 hour group and the reperfusion groups(12,24,48 hours,7 days). The models of vertebrobasilar artery ischemia reperfusion were established via the skull base approach. The auditory function was evaluated by evoked auditory brainstem responses(ABR). Each animal was measured before the operation and after ischemia or ischemia-reperfusion, respectively. Some of the animals were observed the changes of ABR during the ischemia. The slice of temporal bone by means of the Hematoxylin and Eeosin(H&E) staining were used for cochlea histopathology observation.Results After 10～20 minutes the evoked auditory brainstem responses threshold began to increase steadily during verebrobasilar artery ischemia. The changes of ABR during the vertebrobasilar artery ischemia or ischemia-reperfusion consisted of a prolonged in all wave latencies and interpeak latenciesⅠ～Ⅲ, an increase of the auditory threshold,especially 24 hours after ischemia. A statistically significant difference of the auditory threshold shift, interpeak latenciesⅠ～Ⅲ and wave latencies was seen between the groups of ischemia and ischemia-reperfusion. A statistically significant difference was seen between the normal control group and the ischemia and ischemia-reperfusion groups,too.After 1 hour ischemia, outer hair cells(OHCs) were swollen, the vertebrobasilar artery reperfusion could cause more severe lesions of the Corti, spiral ganglion cells(SGCs) and stria vascularis, especially 24、48 hours after ischemia. These studies showed that the disapperance of outer hair cells and the degeneration of spiral ganglion cells. 24、48 hours after reperfusion, the loss of OHCs and the degeneration of SGCs became apparent. Conclusion We had successfully established an animal model of the vertebrobasilar artery ischemia reperfusion in guinea pigs. Vertebrobasilar artery ischemia reperfusion in guinea pigs could cause the lesions of the Corti, spiral ganglion cells(SGCs) and stria vascularis which were more severe in reperfusion injury. Vertebrobasilar artery ischemia reperfusion could delay the latencies of ABR waves, interpeak latenciesⅠ～Ⅲ and increase the threshold.