Abstract

In addition to an endolymphatic hydrops in various models of Ménière's disease, ruptures of the membranes lining the endolymphatic spaces or massive changes in their biochemical permeability are believed to allow large amounts of potassium-rich endolymph to deluge the normally low [K+] perilymphatic fluid. Our clinic has shown that exposure of the lateral and basal membrane parts of living isolated outer hair cells to increasing concentrations of potassium ions resulted in a sustained reversible cellular depolarization. Furthermore, potassium intoxication was accompanied by a strictly longitudinal contraction of the hair cells present. This was followed by hair cell relaxation in the presence of artificial perilymph. These findings suggest a supplementary hypothesis for the clinical manifestations of Ménière's disease: the reversible hair cell depolarization can explain the sudden tinnitus and parts of the hearing loss incurred as well as presumably the vertigo experienced; the reversible longitudinal hair cell contraction induces an abnormal change of cochlear micromechanics, resulting in concomitant attacks of deafness and also possibly contributing to the tinnitus perceived.

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