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两相性内淋巴积水:一种新的动态豚鼠模型。

Two-phase endolymphatic hydrops: a new dynamic guinea pig model.

作者信息

Dunnebier E A, Segenhout J M, Wit H P, Albers F W

机构信息

Department of Otorhinolaryngology, University Hospital Groningen, The Netherlands.

出版信息

Acta Otolaryngol. 1997 Jan;117(1):13-9. doi: 10.3109/00016489709117984.

Abstract

The classical guinea pig model for Meniere's disease, in which endolymphatic hydrops was achieved by destruction of the endolymphatic sac and obliteration of the endolymphatic duct, is a non-physiological profound model with shortcomings in relation to Meniere's disease as seen in patients. We developed a more subtle animal model; the two-phase endolymphatic hydrops. This model is based on a combination of chronic endolymphatic sac dysfunction, induced by slight destruction of the most distal part of the endolymphatic sac, and acute stress-induced endolymph production by stimulation of the Na/K-ATPase in the stria vascularis with aldosterone. Light microscopy of the fluid compartments of four groups of cochleas was used to examine them for the presence of endolymphatic hydrops: i) Normal (control) cochleas showed no hydrops; ii) some of the non-operated (no destruction) aldosterone-treated cochleas showed small degrees of hydrops mainly present in the basal turns; iii) mild dissection of the endolymphatic sac without administration of aldosterone produced a hydrops which was mainly present in the cochlear apex; iv) combination of chronic endolymphatic sac dysfunction and acute attacks of endolymph production by aldosterone administration revealed the most severe degrees of hydrops in all cochlear windings, damage to cochlear structures, and cellular disturbances of the epithelial lining of the endolymphatic sac. This new model may represent a more physiologic and dynamic approach to Meniere's disease and may explain the etiology of many symptoms in patients such as the fluctuant nature and the types of sensoneuronal hearing losses.

摘要

梅尼埃病的经典豚鼠模型是通过破坏内淋巴囊和闭塞内淋巴管来实现内淋巴积水,这是一种非生理性的深度模型,与临床所见的梅尼埃病相比存在缺陷。我们开发了一种更为精细的动物模型;两阶段内淋巴积水模型。该模型基于以下两者的结合:一是通过轻微破坏内淋巴囊最远端诱导慢性内淋巴囊功能障碍,二是用醛固酮刺激血管纹中的钠钾ATP酶急性应激诱导内淋巴生成。使用四组耳蜗的液体腔室的光学显微镜检查内淋巴积水情况:i)正常(对照)耳蜗未显示积水;ii)一些未手术(无破坏)的醛固酮处理的耳蜗显示出轻度积水,主要存在于基底转;iii)对内淋巴囊进行轻度解剖但未给予醛固酮会产生主要存在于耳蜗尖的积水;iv)慢性内淋巴囊功能障碍与醛固酮给药引起的内淋巴生成急性发作相结合,显示所有耳蜗螺旋中积水程度最严重,耳蜗结构受损,内淋巴囊上皮衬里出现细胞紊乱。这种新模型可能代表了一种针对梅尼埃病更具生理性和动态性的方法,并且可以解释患者许多症状的病因,如波动性特征和感觉神经性听力损失的类型。

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