Dunnebier E A, Segenhout J M, Dijk F, Albers F W
Department of Otorhinolaryngology, University Hospital Groningen, The Netherlands.
Otol Neurotol. 2001 Sep;22(5):655-61. doi: 10.1097/00129492-200109000-00017.
The aim of this study was to create a more dynamic animal model of Ménière's disease combining multiple causes, such as the role of endocrine factors and endolymphatic sac dysfunction, that may mimic the fluctuant characteristics of Ménière's disease.
Endolymphatic hydrops remains to be considered a pathologic substrate in the etiology of Ménière's disease. The classic guinea pig model of inducing hydrops by total destruction of the endolymphatic sac is a nonphysiologic rigid model of Ménière's disease.
The authors developed the two-phase endolymphatic hydrops model by inducing hydrops by mild chronic endolymphatic sac dysfunction, in combination with increased endolymph production by aldosterone. Sensory cell damage was evaluated by low-voltage field emission scanning microscopy.
This study describes a wide spectrum of morphologic effects of the outer hair cells in radial gradients, in which most effects were observed in the third to second row of outer hair cells, and longitudinal gradients in which the most severe effects were observed in the apical turns. Most affected were the ears that underwent distal endolymphatic sac dissection followed by the administration of aldosterone. Damaging effects proceeded from degeneration and absence of short stereocilia of outer hair cells and even some inner hair cells in the apical turns, to stereociliary disarrangement and atrophy, followed by degeneration and absence of outer hair cells, which were replaced by supporting cells.
The two-phase endolymphatic hydrops model seems to represent a functional model that may mimic the fluctuant characteristics of Ménière's disease and emphasizes the influence of multiple and coexisting hydrops-inducing influences.
本研究的目的是创建一种更具动态性的梅尼埃病动物模型，该模型结合多种病因，如内分泌因素的作用和内淋巴囊功能障碍，可能模拟梅尼埃病的波动特征。
内淋巴积水仍是梅尼埃病病因学中的一种病理基础。经典的通过完全破坏内淋巴囊来诱导积水的豚鼠模型是一种非生理性的梅尼埃病僵硬模型。
作者通过轻度慢性内淋巴囊功能障碍诱导积水，并结合醛固酮增加内淋巴生成，建立了两阶段内淋巴积水模型。通过低电压场发射扫描显微镜评估感觉细胞损伤。
本研究描述了外毛细胞在径向梯度上的广泛形态学效应，其中大多数效应在外毛细胞的第三排至第二排观察到，以及纵向梯度效应，其中最严重的效应在顶转观察到。受影响最严重的是那些先进行远端内淋巴囊解剖然后给予醛固酮的耳朵。损伤效应从顶转外毛细胞甚至一些内毛细胞的短静纤毛退化和缺失，发展到静纤毛排列紊乱和萎缩，随后外毛细胞退化和缺失，被支持细胞取代。
两阶段内淋巴积水模型似乎代表了一种功能模型，可能模拟梅尼埃病的波动特征，并强调多种并存的积水诱导因素的影响。
