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Cochlear implantation impairs intracochlear microcirculation and counteracts iNOS induction in guinea pigs

Ernst, Benjamin Philipp ; Heinrich, Ulf-Rüdiger ; Fries, Mathias ; Meuser, Regina ; Rader, Tobias ; Eckrich, Jonas ; Stauber, Roland H ; Strieth, Sebastian

Frontiers in cellular neuroscience, 2023-06, Vol.17, p.1189980-1189980 [Periódico revisado por pares]

Switzerland: Frontiers Research Foundation

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  • Título:
    Cochlear implantation impairs intracochlear microcirculation and counteracts iNOS induction in guinea pigs
  • Autor: Ernst, Benjamin Philipp ; Heinrich, Ulf-Rüdiger ; Fries, Mathias ; Meuser, Regina ; Rader, Tobias ; Eckrich, Jonas ; Stauber, Roland H ; Strieth, Sebastian
  • Assuntos: Animals ; Blood flow ; Cerebral blood flow ; Cochlea ; cochlea implantation ; Cochlear implants ; cochlear microcirculation ; Electrodes ; Hearing loss ; hearing preservation ; Hearing protection ; iNOS ; Microscopy ; microvascular permeability ; Microvasculature ; Neuroscience ; Nitric oxide ; Nitric-oxide synthase ; Organ of Corti ; Permeability ; Stria vascularis ; Veins & arteries ; Visual thresholds
  • É parte de: Frontiers in cellular neuroscience, 2023-06, Vol.17, p.1189980-1189980
  • Notas: ObjectType-Article-1
    SourceType-Scholarly Journals-1
    ObjectType-Feature-2
    content type line 23
    These authors have contributed equally to this work and share first authorship
    Reviewed by: Hao Xiong, Sun Yat-sen Memorial Hospital, China; Daogong Zhang, Shandong Provincial ENT Hospital, China; Ivan A. Lopez, University of California, Los Angeles, United States
    Edited by: Yu Sun, Huazhong University of Science and Technology, China
  • Descrição: Preservation of residual hearing remains a great challenge during cochlear implantation. Cochlear implant (CI) electrode array insertion induces changes in the microvasculature as well as nitric oxide (NO)-dependent vessel dysfunction which have been identified as possible mediators of residual hearing loss after cochlear implantation. A total of 24 guinea pigs were randomized to receive either a CI ( = 12) or a sham procedure (sham) by performing a cochleostomy without electrode array insertion ( = 12). The hearing threshold was determined using frequency-specific compound action potentials. To gain visual access to the stria vascularis, a microscopic window was created in the osseous cochlear lateral wall. Cochlear blood flow (CBF) and cochlear microvascular permeability (CMP) were evaluated immediately after treatment, as well as after 1 and 2 h, respectively. Finally, cochleae were resected for subsequent immunohistochemical analysis of the iNOS expression. The sham control group showed no change in mean CBF after 1 h (104.2 ± 0.7%) and 2 h (100.8 ± 3.6%) compared to baseline. In contrast, cochlear implantation resulted in a significant continuous decrease in CBF after 1 h (78.8 ± 8.1%, < 0.001) and 2 h (60.6 ± 11.3%, < 0.001). Additionally, the CI group exhibited a significantly increased CMP (+44.9% compared to baseline, < 0.0001) and a significant increase in median hearing threshold (20.4 vs. 2.5 dB SPL, = 0.0009) compared to sham after 2 h. Intriguingly, the CI group showed significantly lower iNOS-expression levels in the organ of Corti (329.5 vs. 54.33 AU, = 0.0003), stria vascularis (596.7 vs. 48.51 AU, < 0.0001), interdental cells (564.0 vs. 109.1 AU, = 0.0003) and limbus fibrocytes (119.4 vs. 18.69 AU, = 0.0286). Mechanical and NO-dependent microvascular dysfunction seem to play a pivotal role in residual hearing loss after CI electrode array insertion. This may be facilitated by the implantation associated decrease in iNOS expression. Therefore, stabilization of cochlear microcirculation could be a therapeutic strategy to preserve residual hearing.
  • Editor: Switzerland: Frontiers Research Foundation
  • Idioma: Inglês

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