豚鼠椎基底动脉缺血-再灌注对耳蜗损伤的实验研究

目的：探讨椎基底动脉缺血－再灌注耳蜗组织损伤方式有其可能的损伤机制。方法：选用耳廓反射灵敏，体得300－500g的健康杂色豚鼠72只，随机分成6组，即正常对照组，假手术组，缺血30min组，再灌汪1h、6h、24h组。各组动物分别于手术前有处死前分别测试ABR、耳蜗标本HE染色病理检查、耳蜗电镜检查、测定耳蜗组织超氧化物歧化酶（SOD）活力、丙二醛（MDA）含量、耳蜗组织诱导型－氧化氮合酶（iNOS）免疫组化。结果：缺血组及再灌汪各组脑干诱发电位（ABR）发生明显异常，咯波潜伏期明显延长，阈值升高（P＜0．01）；外毛细胞变形，细胞超微结构改变；耳蜗组织MDA含升高、SOD活力降低；iNOS在耳蜗组织表达明显增强。结论：在底动脉缺血－再灌注损伤呵引起豚鼠ABR各波潜伏期延长和阈值增高，可造成耳蜗毛细胞及血管纹等组织病理损伤。耳蜗组织SOD活力下降及MDA升高参与了椎基底动脉缺血－再灌注耳蜗损伤。耳蜗组织在正常情况下，血管纹、毛细胞及螺旋神经节细胞均有iNOS弱阳性表达，在缺血及再灌注期间iNOS表达增强。

Experimental study on cochlea vertebrobasilar artery ischemia reperfusion injury in guinea pigs

Aim: To investigate injuries of the cochlea after the reperfusion of vertebrobasilar ischemia. Methods: Seventy two healthy guinea pigs with positive Preyer's reflex weighted from 300 to 350 g were randomly assigned to 6 groups (n = 12): the normal control group, the sham operation group, the ischemia group and the reperfusion groups. ABR was evaluated, the histomorphology of cochlea and cochlear nucleus were observed, the content of MDA (molondialdehyde) and activity of SOD (superoxide dismutatse) in cochlea were measured, and the iNOS im-munoactivity in cochlea was studied. Results: The prolonged latencies and gradual elevation of the thresholds were clearly seen in the ischemia group and reperfusion groups. Lesions were detected in the hair cell and the stria vascu-laris, the SOD activities decreased, and MDA concentrations increased, labeling expression of iNOS increased significantly. Conclusions: 'The vertebrobasilar artery ischemia reperfusion injury(VIRI) can increase the latency of ABR waves and threshold in guinea pigs. The VIRI can cause the lesions of the corti and the stria vascularis which are more severe in reperfusion injury, and cause the decrease of SOD activities and increase of MDA contents of cochlea. There is slightly positive expression of iNOS in the hair cell, the stria vascularis, and the spiral ganglion in normal cochlea tissues. The expression of iNOS increased with the severity of ischemia reperfusion.