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The effects of isosorbide on distortion-product otoacoustic emissions (DPOAEs) and endocochlear DC potential (EP) were examined in experimentally induced endolymphatic hydropic ears and untreated control ears using 20 albino guinea pigs. DPOAEs and EP in the hydropic ears decreased after obliteration of the endolymphatic duct and sac. The administration of isosorbide restored DPOAEs to the normal level, whereas EP was further reduced. In control ears there was no significant change in DPOAEs and EP after the administration of isosorbide. The results obtained in the present study indicate that the effect of isosorbide on DPOAEs is different from that on EP, and the recovery of DPOAEs in hydropic ears is not a secondary phenomenon due to the recovery of EP.

The endocochlear potential (EP) was measured in 38 guinea pigs with experimentally induced endolymphatic hydrops at the 3rd, 6th, 12th and 24th postoperative weeks, and the effects of furosemide (FUR, 50 or 80 mg/kg) on the EP were examined. A time-related reduction of the EP from the normal value and increased susceptibility to FUR were disclosed in the hydropic animals. Furthermore, 24-week animals given 80 mg/kg FUR showed a significantly slower recovery rate of the EP than the other groups, indicating impairment of the strial function progressive with post-operative time. The negative component of the EP was considered to be unimpaired until at least 12 weeks after the surgery.

In this paper the current state of knowledge of the development in experimental endolymphatic hydrops (EEH) is summarized, with particular emphasis on calcium. An imbalanced Ca2+ homeostasis in the inner ear is demonstrated using EEH as an animal model for Meniere's disease. The possibility of a receptor-mediated Ca2+ transport across the epithelial layer, especially the light cells, and of 'chemical signal' as an initiating modulating factor in the disturbance of Ca2+ homeostasis was suggested. It is pointed out that melanin is capable of binding calcium and may act as a buffering system. Finally, the possible malfunction of the Ca-overloaded melanocytes on the inner ear function is discussed.

We have previously shown by chronic implantation of round window electrodes, that after the experimental induction of endolymphatic hydrops by surgical blockade of the endolymphatic canal, in the guinea pig, there is a low/mid-frequency fluctuant hearing loss, followed by a very high frequency loss and after a few months the audiogram is flat. This evolution reproduces exactly that observed in Meniere's patients. The aim of this study was to investigate the evolution of one aspect of vestibular function in parallel with audiogram changes. The nystagmic responses in the dark were tested every month during the 4 months which followed hydrops induction. There was considerable variation in the number of evoked saccades for different control animals and even between different recordings for the same control animal. However, in general, the number of saccades to right and left rotation was symmetrical for control animals, whereas for hydropic animals there was a period, within the first 2 months post-operation, when there was a reduction of saccades to the left (operated side) with sometimes an increase to the right. This asymmetry which occurred in the period of fluctuant hearing losses did not however appear synchronized with audiogram fluctuations. The nystagmic responses tended to become symmetrical over the 4 months post-operation. Oral administration of glycerol to animals whose nystagmus was asymmetric brought the vestibular response towards symmetry in 50% of the cases. Although episodes of vertigo, as known in Meniere's disease, were never observed in operated guinea pigs, these data indicate that they have some functional vestibular disturbance.

The inner ear possesses remarkably stable homeostatic mechanisms for the maintenance of the functional integrity of the inner ear end-organs. The inner ear fluid maintains its homeostasis by a variety of subtle regulatory mechanisms, both locally and systemically. Any disturbance in one of these mechanisms can induce the disruption of homeostasis expressed by ionic, osmotic, or metabolic imbalance between the compartments. This can be manifested as membrane displacement or abnormal functions of the inner ear, depending on the degree of the disturbance. Further studies are necessary to clarify these regulatory mechanisms of homeostasis and those conditions which alter homeostasis which can result in the abnormal functions. Further research along this line is essential in order to understand the etiology of endolymphatic hydrops and also to establish guidelines for possible normalization of this pathological status.

Fluctuation of hearing at low frequencies is one of the most characteristic findings in Meniere's disease and seems to be a phenomenon closely related to changes of endolymphatic pressure and volume. In the present study, pressure was applied to the external auditory canal of patients with Meniere's disease, and the effect on the bone conduction threshold was examined at times of depressed and improved hearing. In more than half of these cases, it was found that the pressure effect was marked at the time of improved hearing acuity, but not at the time of depressed hearing. This effect was also confirmed in more objective experiments with guinea pigs. It is concluded that the fluctuation of hearing in Meniere's disease seems to be a phenomenon accompanying the endolymphatic pressure change in the scala media.