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We conducted both histopathological and functional assessment of the vestibular system in the guinea-pig. Since the milestone findings on the temporal bones of MD patients,1, 2 endolymphatic hydrops (EH) has been considered as the histopathological origin of MD, as characteristic morphological changes were reported to be produced by surgical obstruction of the endolymphatic sac (ES) in guinea-pig.3 This observation indicates that malabsorption of endolymph in the ES is one of the possible mechanisms underlying the development of EH. In the first experiment, all animals were maintained 1 or 4 weeks after electrocauterization of the endolymphatic sac of the left ear and were given either saline or desmopressin (vasopressin type 2 receptor agonist). This experimentally induced EH has been frequently used as an animal model to investigate the pathogenesis of inner ear disorders associated with EH.
The temporal bones from both ears were harvested and the extent of endolymphatic hydrops was quantitatively assessed. In the second experiment, either 1 or 4 weeks after surgery, animals were assessed for balance disorders and nystagmus after the administration of saline or desmopressin. EH is considered to be the result of disruption of inner ear water homeostasis, which involves excessive production of endolymph and/or reduced absorption of endolymph. In the first experiment, the proportion of endolymphatic space in the cochlea and the saccule was significantly greater in ears that survived for 4 weeks after surgery and were given desmopressin compared with other groups. Until recently, however, the detailed mechanisms underlying the overaccumulation of endolymph were unclear. Membranous hydrops in the inner ear of the guinea pig after the obliteration of the endolymphatic sac. In the second experiment, all animals that underwent surgery and were given desmopressin showed spontaneous nystagmus and balance disorder, whereas all animals that had surgery but without desmopressin administration were asymptomatic. Since the discovery of aquaporin (AQP) water channels,7 it has been proposed that precise regulation of water reabsorption largely depends on the regulation of AQP2 channels and that water permeability can change rapidly in response to vasopressin(VP).8 Recently, it has come to light that this mechanism has a crucial role not only in the kidney but also in the inner ear.
Our animal model induced severe endolymphatic hydrops in the cochlea and the saccule, and showed episodes of balance disorder along with spontaneous nystagmus. Experiment 1 was designed to investigate the influence of desmopressin on the development of EH morphologically. Experiment 2 was designed to investigate the role of desmopressin on changes in vestibular function. Time course of vestibular function changes of experimental endolymphatic hydrops in guinea pigs. The animals used in Experiment 1 were albino outbred English short-haired guinea-pig (Hartley).
All animals underwent electrocauterization of the ES of the left ear as reported previously.21, 22 The right ear was not treated surgically. The surgical procedures are described below (in the Surgical procedure for electrocauterization of the ES section). Twelve animals were allocated to survive for 1 week after electrocauterization of the ES and the other 12 for 4 weeks. Acupuncture , heat , electrical stimulation channels of energy , body's internal organs, correct imbalances digestion, absorption, and energy production activities, circulation of their energy .
In either group, six animals were given saline and the remaining six were treated with desmopressin systemically 1 h before euthanasia.
All animals were killed under deep anesthesia using ketamine and xylazine, and the temporal bones were collected from both sides. All animals underwent electrocauterization of the endolymphatic sac (ES) and duct on the left side and were randomly divided into two groups of either 1 or 4 weeks survival.
Subsequently, they were placed in a prone position with a head holder and underwent dorsal midline scalp incision.
The left occipital bone was removed for visual exposure of the ES via an epidural occipital approach. Thereafter, the extraosseous portion of the sac was cauterized electrically with a bipolar electrocoagulator (Surgitron Model FFPF; Ellman International, Hewlett, NY, USA) so as not to injure the sigmoid sinus. The temporal bones were removed on both sides and postfixed in 10% formalin solution for 7 days.


Expressions of aquaporin-2, vasopressin type 2 receptor, transient receptor potential channel vanilloid (TRPV)1, and TRPV4 in the human endolymphatic sac.
Subsequently, the specimens were decalcified in ethylenediamine tetraacetic acid for 14 days, and then dehydrated in a graded ethanol series before being embedded in paraffin.
The prepared blocks were cut horizontally parallel to the axis of the modiolus into 6-μm sections. The sections were stained with hematoxylin and eosin for observation under a light microscope. We examined the degree of EH in the cochleae, vestibules, and semicircular canals using digital image measurement software, Micro Analyzer Ver. Expression of aquaporins and vasopressin type 2 receptor in the stria vascularis of the cochlea. To assess quantitatively the endolymphatic space variations across the cochlea turns, we measured the increase in the ratio of the cross-sectional area of the scala media (IR-S) in the basal, second, third, and apical turns, excluding the hook portion at the mid-modiolar sections. For this analysis, we used the following two parameters: (1) the cross-sectional area of the dilated scala media (Figure 2a, gray area), and (2) the cross-sectional area of the original scala media, enclosed by a straight line segment (Figure 2a, black area). This line segment represents the normal position of Reissner’s membrane at the upper margin of the stria vascularis and its normal medial attachment at the spiral limbus. In the utricle, we also examined the proportion of the area of the utricle (Figure 2c, gray area) to that of the labyrinth (Figure 2c, black area) in the horizontal section including the crista of the lateral semicircular canal. Localization, frequency and severity of endolymphatic hydrops and the payhology of the labyrinthine membrane in Meniere’s disease.
We compare the differences in the mean values among each group with Tukey’s multiple comparison test. Sixteen animals underwent electrocauterization of the ES in the left ear, and the remaining eight animals received no surgical procedure. The 16 animals that underwent surgery were divided into two groups, which were maintained for 1 week or 4 weeks before administration of saline or desmopressin. In either group, four animals were given saline and the remaining four animals were given desmopressin. Specialization, Materia Medica, internal medicine, diagnosis , examine, refer ,investigations .health shops, pharmacies, prescription, complex remedies, labelled ,individualized ,mental, migraines, asthma, eczema, hay fever, glandular fever, chronic fatigue syndrome. Computed radiographic measurement of the dimensions of the vestibular aqueduct in Meniere’s disease. Free-radical, toxin-, inflammatory, degenerative diseases, Nutrients, minerals, enzymes, vitamins, amino acids.
We also monitored posture for 1 h after the administration of saline or desmopressin to determine the presence or absence of a balance disorder. Time-realted changes in cochlear potentials in guinea pigs with experimentally induced endolymphatic hydrops.
In the 4 W Combined group, the saccular space was markedly extended and the saccular membrane was widely adhered to the stapes footplate (Figure 4d). In the Surgery ear group, the scala media is distended and shows moderate hydrops (arrowhead). Time course changes of vasopressin-induced enlargement of the rat intrastrial space and the effects of a vasopressin type 2 antagonist. Pathophysiology of Meniere’s syndrome: are symptoms caused by endolymphatic hydrops? In the Combined ear group, severe saccular hydrops has extended to press against the stapes footplate (arrow).Full figure and legend (335K)Figure 5 shows the results of quantitative analyses of the changes in the endolymphatic space in the cochlea, saccule, utricle, and the semicircular canal. Association between endolymphatic hydrops as revealed by magnetic resonance imaging and caloric response.
In the Combined group, EH appeared to develop within 1 h of desmopressin administration.
Vasopressin in definite Meniere’s disease with positive electrocochleographic findings.


The development and clinical application of a new radioimmunoassay for arginine–vasopressin in human plasma.
Expression of mRNA encoding vasopressin V1a, vasopressin V2, and ANP-B receptors in the rat cochlea.
After the administration of desmopressin, one animal in the V-Desmopressin group demonstrated spontaneous nystagmus.
Effects of lithium on endolymph homeostasis and experimentally induced endolymphatic hydrops.
In cases 2, 6, and 7, the direction of nystagmus changed from the left to the right, indicating a change from irritative nystagmus to paralytic nystagmus. The amplitude and direction of the maximum slow-phase velocity varied among the animals.Top of pageDISCUSSIONIn this investigation, we successfully developed a new clinically relevant animal model for MD, in which desmopressin was administered after electrocauterization of the ES.
In this animal model, distinct EH was evident in the cochlea and saccule, whereas there were no obvious changes in the utricle or semicircular canals. Temporal bone studies of patients with MD have revealed that EH is more frequently observed in the pars inferior than in the pars superior of the inner ear. The EH of their model is thought to involve retention hydrops caused by the obliteration of the endolymphatic duct. Episodes of temporary imbalance or vertigo, which are typical features of patients with MD, have not however been reported in animals that underwent obliteration of their ES. Therefore, such animals with EH due only to the retention of endolymph are not considered suitable as an animal model of MD.Considering these issues, we speculated that the lack of temporary vestibular episodes in the classical MD animal model might be related to growth rates of formation of EH, not the degree of EH. That is, the development of EH caused by malabsorption in the ES is too slow to produce a vertiginous attack.
Indeed, animals that survived for 4 weeks after electrocauterization of the left ES (4 W Surgery group) developed severe EH in the cochlea and the saccule, but showed no distinct vestibular disorders. Thus, the disorders of vestibular function could not be rationalized on the basis of the degree of EH.
On the other hand, EH in animals administered desmopressin is thought to develop as rapidly as within 1 h. Analysis of the average growth rates of EH development, estimated from the IR and proportion of saccular space, indicates that animals in the Combined groups had very high growth rates of EH development both in the cochlea and in the saccule, regardless of the survival time between surgery and the measurement.
Hornibrool et al40 reported that there have not been abnormal plasma levels of arginine VP in patients of MD. The reasons for these controversial results might have been that because platelets present in plasma cause overestimation of plasma arginine VP and partly to avoid degradation of AVP activity resulting from its short half-life,41, 42, 43 it might be one of the most important reasons for the great differences in basal arginine VP concentrations observed in different laboratories. These previous experimental findings indicate that the water homeostasis of the inner ear fluid is partly regulated via the VP–AQP2 system.
We speculate that under chronic endolymphatic dysfunction, it may reduce absorption of endolymph and chemical mechanisms can concomitantly cause Meniere’s symptoms. Chemical factors include hydrostatic pressure alterations, it changes membrane permeability, causing inappropriate ion across the membrane barrier so as to incite sensory dendrites and lead to cochlear and vestibular symptoms. In our experiment, we can see a remarkable histopathological change in the cochlea and saccule, not in the utricle and semicircular canals.
There remains some discussion about whether an endolymph–perilymph pressure gradient may cause these morphological variations.
Therefore, the difference in AQP2 expression in the stria vascularis and the dark cells may cause morphological variations. Further study is needed to determine the mechanism of the VP–AQP2 system in the inner ear using this animal model to understand the relationship between VP and MD.



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