The Effect of Endolymphatic Hydrops and Mannitol Dehydration Treatment on Guinea Pigs

Abstract

BackgroundEndolymphatic hydrops (EH) is considered as the pathological correlate of Menière’s disease (MD) and cause of hearing loss. The mechanism of EH, remaining unrevealed, poses challenges for formalized clinical trials.ObjectiveThis study aims to investigate the development of hearing loss, as well as the effect of dehydration treatment on EH animal models.MethodsIn this study, different severity EH animal models were created. The laser Doppler vibrometer (LDV) and auditory brainstem responses (ABR) were used to study the effects of EH and the dehydration effects of mannitol. The LDV was used to measure the vibration of the round window membrane (RWM) reflecting the changes in inner ear impedance. ABR was used to evaluate the hearing changes. Furthermore, tissue section and scanning electron microscopy (SEM) observations were used to analyze the anatomical change to the cochlea and outer hair cells.ResultsThe RWM vibrations decreased with the severity of EH, indicating an increase in the cochlear impedance. The dehydration therapy lowered the impedance to restore acoustic transduction in EH 10- and 20-day animal models. Simultaneously, the ABR thresholds increased in EH models and were restored after dehydration. Moreover, a difference in the hearing was found between ABR and LDV results in severe EH animal models, and the dehydration therapy was less effective, indicating a sensorineural hearing loss (SNHL).ConclusionEndolymphatic hydrops causes hearing loss by increasing the cochlear impedance in all tested groups, and mannitol dehydration is an effective therapy to restore hearing. However, SNHL occurs for the EH 30-day animal models, limiting the effectiveness of dehydration. Our results suggest the use of dehydrating agents in the early stage of EH.

Why should multiple dehiscences of the otic capsule be considered before surgically treating patients with superior semicircular canal dehiscence? A radiological monocentric review and a case series

“…A possible explanation of the postsurgical hearing loss observed in these two cases could be that the SSCD plugging reduced the volume of the endolymphatic space, generating a hyper-pressure in the membranous cochlear canal and, thus, a significant auditory transduction disruption. This assumption is in accordance with the results of experimental animal models of hydrops ( 27 , 28 ). Moreover, the apparition of hyper-pressure in the endolymphatic system that seemed to manifest itself immediately after plugging is also supported by the two following cases in which signs of vestibular hydrops were evident.…”

Association of Fibrinogen Levels with Sudden Sensorineural Hearing Loss Incidence and Prognosis: a Meta-Analysis

“…It is undoubtedly important to identify the underlying cause of SSNHL since the treatment modalities may differ between different etiologies. For instance, SSNHL due to endolymphatic hydrops may require dehydration of the endolymph whereas SSNHL due to hyper brinogenemia may require steroid and de brinogenation treatment 44,45 .…”

G protein-coupled receptors in cochlea: Potential therapeutic targets for hearing loss

“…V2R is thought to play a role in endolymphatic hydrops (EH). EH is caused by an imbalance in the volume of endolymph and is thought to be associated with the pathology of Menière’s disease (MD) that is a kind of hearing loss’s inner ear disease ( Zou et al, 2019 ; Wang et al, 2022 ). EH can be also inhibited via reducing the expression of V2R.…”

“…In addition, there is some work to correct RHO mutations by CRISPR/Cas9 gene editing for the treatment of inherited retinal degeneration ( Bakondi et al, 2016 ; Burnight et al, 2017 ). Among the nine genes with mutations or deletions of GPCR-encoding genes that cause hearing loss, including GABA B1 ( Maison et al, 2009 ), GPR156 ( Kindt et al, 2021 ), mGluR7 ( Friedman et al, 2009 ), VLGR1 ( Kimberling et al, 1995 ), PAC1R ( Ruel et al, 2021 ), EDNRB ( Huang et al, 2021 ), S1PR2 ( Santos-Cortez et al, 2016 ), TSHR ( Li et al, 1999 ), and CRFR1 ( Graham and Vetter, 2011 ), five of them mGluR7 ( Friedman et al, 2009 ), VLGR1 ( Kimberling et al, 1995 ), EDNRB ( Huang et al, 2021 ), V2R ( Zou et al, 2019 ; Wang et al, 2022 ), and S1PR2 ( Santos-Cortez et al, 2016 ) are directly related to human deafness, which are especially worth developing for gene therapy.…”