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Hydrogen Gas Inhalation Attenuates Acute Impulse Noise Trauma: A Preclinical In Vivo Study

OBJECTIVE: Molecular hydrogen (H(2)) has shown therapeutic potential in several oxidative stress-related conditions in humans, is well-tolerated, and is easily administered via inhalation.The aim of this preclinical in vivo study was to investigate whether impulse noise trauma can be prevented by H(...

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Autores principales: Videhult Pierre, Pernilla, Fransson, Anette, Kisiel, Marta A., Laurell, Göran
Formato: Online Artículo Texto
Lenguaje:English
Publicado: SAGE Publications 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10315859/
https://www.ncbi.nlm.nih.gov/pubmed/35962590
http://dx.doi.org/10.1177/00034894221118764
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author Videhult Pierre, Pernilla
Fransson, Anette
Kisiel, Marta A.
Laurell, Göran
author_facet Videhult Pierre, Pernilla
Fransson, Anette
Kisiel, Marta A.
Laurell, Göran
author_sort Videhult Pierre, Pernilla
collection PubMed
description OBJECTIVE: Molecular hydrogen (H(2)) has shown therapeutic potential in several oxidative stress-related conditions in humans, is well-tolerated, and is easily administered via inhalation.The aim of this preclinical in vivo study was to investigate whether impulse noise trauma can be prevented by H(2) when inhaled immediately after impulse noise exposure. METHODS: Guinea pigs (n = 26) were subjected to impulse noise (n = 400; 156 dB SPL; 0.33/s; n = 11; the Noise group), to impulse noise immediately followed by H(2) inhalation (2 mol%; 500 ml/min; 1 hour; n = 10; the Noise + H(2) group), or to H(2) inhalation (n = 5; the H(2) group). The acoustically evoked ABR threshold at 3.15, 6.30, 12.5, 20.0, and 30.0 kHz was assessed before and 4 days after impulse noise and/or H(2) exposure. The cochleae were harvested after the final ABR assessment for quantification of hair cells. RESULTS: Noise exposure caused ABR threshold elevations at all frequencies (median 35, 35, 30, 35, and 35 dB SPL, the Noise group; 20, 25, 10, 13, and 20 dB SPL, the Noise + H(2) group; P < .05) but significantly less so in the Noise + H(2) group (P < .05). Outer hair cell (OHC) loss was in the apical, mid, and basal regions 8.8%, 53%, and 14% in the Noise group and 3.5%, 22%, and 1.2% in the Noise + H(2) group. The corresponding inner hair cell (IHC) loss was 0.1%, 14%, and 3.5% in the Noise group and 0%, 2.8%, and 0% in the Noise + H(2) group. The difference between the groups was significant in the basal region for OHCs (P = .003) and apical (P = .033) and basal (P = .048) regions for IHCs. CONCLUSIONS: Acute acoustic trauma can be reduced by H(2) when inhaled immediately after impulse noise exposure.
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spelling pubmed-103158592023-07-04 Hydrogen Gas Inhalation Attenuates Acute Impulse Noise Trauma: A Preclinical In Vivo Study Videhult Pierre, Pernilla Fransson, Anette Kisiel, Marta A. Laurell, Göran Ann Otol Rhinol Laryngol Original Articles OBJECTIVE: Molecular hydrogen (H(2)) has shown therapeutic potential in several oxidative stress-related conditions in humans, is well-tolerated, and is easily administered via inhalation.The aim of this preclinical in vivo study was to investigate whether impulse noise trauma can be prevented by H(2) when inhaled immediately after impulse noise exposure. METHODS: Guinea pigs (n = 26) were subjected to impulse noise (n = 400; 156 dB SPL; 0.33/s; n = 11; the Noise group), to impulse noise immediately followed by H(2) inhalation (2 mol%; 500 ml/min; 1 hour; n = 10; the Noise + H(2) group), or to H(2) inhalation (n = 5; the H(2) group). The acoustically evoked ABR threshold at 3.15, 6.30, 12.5, 20.0, and 30.0 kHz was assessed before and 4 days after impulse noise and/or H(2) exposure. The cochleae were harvested after the final ABR assessment for quantification of hair cells. RESULTS: Noise exposure caused ABR threshold elevations at all frequencies (median 35, 35, 30, 35, and 35 dB SPL, the Noise group; 20, 25, 10, 13, and 20 dB SPL, the Noise + H(2) group; P < .05) but significantly less so in the Noise + H(2) group (P < .05). Outer hair cell (OHC) loss was in the apical, mid, and basal regions 8.8%, 53%, and 14% in the Noise group and 3.5%, 22%, and 1.2% in the Noise + H(2) group. The corresponding inner hair cell (IHC) loss was 0.1%, 14%, and 3.5% in the Noise group and 0%, 2.8%, and 0% in the Noise + H(2) group. The difference between the groups was significant in the basal region for OHCs (P = .003) and apical (P = .033) and basal (P = .048) regions for IHCs. CONCLUSIONS: Acute acoustic trauma can be reduced by H(2) when inhaled immediately after impulse noise exposure. SAGE Publications 2022-08-12 2023-08 /pmc/articles/PMC10315859/ /pubmed/35962590 http://dx.doi.org/10.1177/00034894221118764 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/This article is distributed under the terms of the Creative Commons Attribution 4.0 License (https://creativecommons.org/licenses/by/4.0/) which permits any use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).
spellingShingle Original Articles
Videhult Pierre, Pernilla
Fransson, Anette
Kisiel, Marta A.
Laurell, Göran
Hydrogen Gas Inhalation Attenuates Acute Impulse Noise Trauma: A Preclinical In Vivo Study
title Hydrogen Gas Inhalation Attenuates Acute Impulse Noise Trauma: A Preclinical In Vivo Study
title_full Hydrogen Gas Inhalation Attenuates Acute Impulse Noise Trauma: A Preclinical In Vivo Study
title_fullStr Hydrogen Gas Inhalation Attenuates Acute Impulse Noise Trauma: A Preclinical In Vivo Study
title_full_unstemmed Hydrogen Gas Inhalation Attenuates Acute Impulse Noise Trauma: A Preclinical In Vivo Study
title_short Hydrogen Gas Inhalation Attenuates Acute Impulse Noise Trauma: A Preclinical In Vivo Study
title_sort hydrogen gas inhalation attenuates acute impulse noise trauma: a preclinical in vivo study
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10315859/
https://www.ncbi.nlm.nih.gov/pubmed/35962590
http://dx.doi.org/10.1177/00034894221118764
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