A new aspect in pathogenesis of experimental hydrops: role of calcium.
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.
Meyer zum Gottesberge
A M
AM
Laboratory of Experimental Otology and Physiology, ENT Clinic, University of Düsseldorf, Federal Republic of Germany.
Ninoyu
O
O
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D007758:Ear, Inner / Q000473:pathology; D004710:Endolymph / Q000502:physiology; D006168:Guinea Pigs; D006706:Homeostasis; D008297:Male; D008575:Meniere Disease / Q000209:etiology* / Q000473:pathology; D008854:Microscopy, Electron; D009041:Motion Sickness / Q000209:etiology*; D009997:Osmotic Pressure; D013026:Space Flight
D002118:Calcium