Abstract
Objective: Exposure to loud noise can impair cochlear microcirculation and cause noise-induced hearing loss (NIHL). TNF-α signaling has been shown to be activated in NIHL and to control spiral modiolar artery vasoconstriction that regulates cochlear microcirculation. It was the aim of this experimental study to analyse the effects of the TNF-α inhibitor etanercept on cochlear microcirculation and hearing threshold shift in NIHL in vivo. Design: After assessment of normacusis using ABR, loud noise (106 dB SPL, 30 minutes) was applied on both ears in guinea pigs. Etanercept was administered systemically after loud noise exposure while control animals received a saline solution. In vivo fluorescence microscopy of strial capillaries was performed after surgical exposure of the cochlea for microcirculatory analysis. ABR measurements were derived from the contralateral ear. Study sample: Guinea pigs (n = 6, per group). Results: Compared to controls, cochlear blood flow in strial capillary segments was significantly increased in etanercept-treated animals. Additionally, hearing threshold was preserved in animals receiving the TNF-α inhibitor in contrast to a significant threshold raising in controls. Conclusions: TNF-α inhibition using etanercept improves cochlear microcirculation and protects hearing levels after loud noise exposure and appears as a promising treatment strategy for human NIHL.
Acknowledgements
We thank Dr. Tania M. Welzel, for critical proof-reading of the manuscript.
Declaration of interest: This study was supported by grants by DAAD (W.A., Deutscher Akademischer Austauschdienst, Bonn, Germany), Friedrich-Baur-Foundation (Munich, Germany), and Else Kroener-Fresenius-Foundation (Bad Homburg, Germany). The authors report no declarations of interest.
This study was presented at the 83rd Annual Meeting of the German Society of Otolaryngology, Head & Neck Surgery, May 16–20, 2012, Mainz, Germany (German Medical Science (GMS) Publishing House, 2012. Doc12hnod544; Title: Effekt einer TNF-α-Inhibition auf Mikrozirkulation und Hörfunktion des Innenohres nach akuter Lärmschädigung).