[Experimental model of endolymphatic hydrops].

We have investigated by electrophysiology, morphology and pharmacology, the consequences of the surgical blocking of the endolymphatic duct in the guinea pig. We have demonstrated an immediate fluctuant CAP sensitivity loss on the low frequencies. Some weeks later a very high frequency loss can also be detected and finally after several months the mid frequencies are also affected and audiogram becomes relatively flat. This type of evolution of sensitivity loss corresponds remarkably well to the type of evolution of hearing loss observed in Ménière's patients. We have demonstrated that the early low frequency fluctuant losses are almost certainly a result of the selective atrophy of the short and middle stereocilia on the outer hair cells in the upper three cochlear turns, corresponding to a new hait cell pathology. Since ion channels are likely to be localised close to inter-stereocilia, row tip links this type of stereocilia atrophy could account for the low frequency fluctuant CAP sensitivity losses in hydropic cochleas. In addition this type of atrophy recalls a retrograde step in the ontogenesis of hair cells. Application of hydrostatic pressure directly to the endolymph via the endolymphatic duct provoked a high frequency sensitivity loss suggesting that endolymphatic pressure might be implicated in the late phase in the evolution of the hearing loss. Long-terme treatment by the diuretic chlorthalidone appeared to slow down the evolution of early low frequency CAP sensitivity loss and could reduce the volume of the hydrops. However in the long-term the CAP sensitivity loss was not arrested.(ABSTRACT TRUNCATED AT 250 WORDS)