Meyer zum Gottesberge A M, Ninoyu O
Laboratory of Experimental Otology and Physiology, ENT Clinic, University of Düsseldorf, Federal Republic of Germany.
Aviat Space Environ Med. 1987 Sep;58(9 Pt 2):A240-6.
An imbalanced Ca++-homeostasis in the inner ear was demonstrated using an animal model for Menière's disease (MD). An increase of Ca++ concentration in the endolymph, as well as in some cells of the inner ear tissue, causes a rise of osmotic pressure and decrease of electric potential. Based on these results, we assume a new aspect in the pathophysiology of MD. It is proposed that the common denominator of MD, experimental endolymphatic hydrops (EEH), and space motion sickness (SMS) is primarily a shift of the inner ear Ca++ homeostasis towards a higher concentration of free Ca++ in the fluid compartments and adjacent intracellular spaces. It is postulated that an increase of Ca++ in this system might affect the transduction process and other functions associated with Ca++, such as turnover of otoconia.
利用梅尼埃病（MD）动物模型证明了内耳中钙稳态失衡。内淋巴以及内耳组织中某些细胞内钙离子浓度的增加会导致渗透压升高和电位降低。基于这些结果，我们推测MD病理生理学有一个新的方面。有人提出，MD、实验性膜迷路积水（EEH）和空间运动病（SMS）的共同特征主要是内耳钙稳态向内耳液腔和相邻细胞内空间中游离钙离子浓度升高的方向转变。据推测，该系统中钙离子的增加可能会影响转导过程以及与钙离子相关的其他功能，如耳石的周转。
