Harada T
Department of Otolaryngology, Osaka University Medical School.
Nihon Jibiinkoka Gakkai Kaiho. 1990 Aug;93(8):1227-40. doi: 10.3950/jibiinkoka.93.1227.
Complement is known to relate to many inflammatory reactions. C4a, C3a and C5a, known as anaphylatoxins, are known to cause strong inflammatory reactions. In this study, the role of anaphylatoxins on the pathogenesis in the cochlea was examined. On hundred forty six male Harley guinea pigs, weighing about 350 grs, all susceptible to preyer's reflex, were used in this study. Anaphylatoxins were made from guinea pig serum treated with zymosan, and inoculated into the carotid artery of the guinea pigs. Parts of these animals were sacrificed and examined at ten minutes, one day, two days, three days, seven days, ten days and fifteen days after injection of anaphylatoxins. Pathological changes in inner ears were observed by light microscopy. After 10 minutes, inner ears were found morphologically normal. After one day, inner ears were found to be almost morphologically normal but the stria vascularis was observed with cystic formation. After two days, cystic formations in the stria vascularis were enlarged and Reissner's membranes were collapsed in some other animals. After three days, the stria vascularis in the various cochlear turns except in the basal turn, were extremely atrophied, some cochlear nerves showed degeneration and some cochlea showed endolymphatic hydrops. After seven days, ten days and fifteen days, the morphological changes showed atrophy in the stria vascularis similar to the results observed on the third days. Atrophy in the stria vascularis was improved gradually with time, but the degeneration of the cochlear nerve was not improved. Opinions have been divided on the cause of inner ear disease including Meniere's disease. Many authors have reported that infectious diseases, for example mumps, measles and cytomegalovirus infection, have caused human sensorineural hearing loss. These diseases have been reported to result in atrophy in the stria vascularis, degeneration of the cochlear nerve and some other pathological changes. In this study, it was clearly observed that the atrophy of the stria vascularis, the endolymphatic hydrops and other morphological changes were caused by introduction of anaphylatoxins. These results were similar to the pathological changes observed in inner ear diseases in human beings. Therefore, inflammatory substances, including anaphylatoxins, were closely related to the cause of inner ear diseases. The animal model used in this report is considered to be important for elucidating the pathogenesis of inner ear diseases.
已知补体与许多炎症反应相关。C4a、C3a和C5a被称为过敏毒素,已知会引发强烈的炎症反应。在本研究中,研究了过敏毒素在耳蜗发病机制中的作用。本研究使用了146只雄性哈雷豚鼠,体重约350克,均对普赖尔反射敏感。过敏毒素由经酵母聚糖处理的豚鼠血清制成,并接种到豚鼠的颈动脉中。在注射过敏毒素后的10分钟、1天、2天、3天、7天、10天和15天,处死部分动物并进行检查。通过光学显微镜观察内耳的病理变化。10分钟后,内耳在形态上正常。1天后,内耳在形态上几乎正常,但观察到血管纹有囊肿形成。2天后,血管纹中的囊肿形成扩大,在其他一些动物中观察到Reissner膜塌陷。3天后,除基底转外,各耳蜗转的血管纹极度萎缩,一些耳蜗神经出现退变,一些耳蜗出现内淋巴积水。7天、10天和15天后,形态学变化显示血管纹萎缩,与第3天观察到的结果相似。血管纹的萎缩随时间逐渐改善,但耳蜗神经的退变没有改善。关于包括梅尼埃病在内的内耳疾病的病因存在不同观点。许多作者报告说,传染病,如腮腺炎、麻疹和巨细胞病毒感染,会导致人类感音神经性听力损失。据报道,这些疾病会导致血管纹萎缩、耳蜗神经退变和其他一些病理变化。在本研究中,清楚地观察到血管纹萎缩、内淋巴积水和其他形态学变化是由过敏毒素的引入引起的。这些结果与人类内耳疾病中观察到的病理变化相似。因此,包括过敏毒素在内的炎症物质与内耳疾病的病因密切相关。本报告中使用的动物模型被认为对阐明内耳疾病的发病机制很重要。