Acute intermittent hypoxia evokes ventilatory long-term facilitation and active expiration in unanesthetized rats

Detalhes bibliográficos
Autor(a) principal: Mendonça-Junior, Bolival A. [UNESP]
Data de Publicação: 2021
Outros Autores: V. Fernandes, Marcos [UNESP], Zoccal, Daniel B. [UNESP]
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNESP
Texto Completo: http://dx.doi.org/10.1016/j.resp.2021.103768
http://hdl.handle.net/11449/229254
Resumo: Acute intermittent hypoxia (AIH) modifies the functioning of the respiratory network, causing respiratory motor facilitation in anesthetized animals and a compensatory increase in pulmonary ventilation in freely behaving animals. However, it is still unclear whether the ventilatory facilitation induced by AIH in unanesthetized animals is associated with changes in the respiratory pattern. We found that Holtzman male rats (80–150 g) exposed to AIH (10 × 6% O2 for 30–40 s every 5 min, n = 9) exhibited a prolonged (30 min) increase in baseline minute ventilation (P < 0.05) compared to control animals (n = 13), combined with the occurrence of late expiratory peak flow events, suggesting the presence of active expiration. The increase in ventilation after AIH was also accompanied by reductions in arterial CO2 and body temperature (n = 5–6, P < 0.05). The systemic treatment with ketanserin (a 5-HT2 receptor antagonist) before AIH prevented the changes in ventilation and active expiration (n = 11) but potentiated the hypothermic response (n = 5, P < 0.05) when compared to appropriate control rats (n = 13). Our findings indicate that the ventilatory long-term facilitation elicited by AIH exposure in unanesthetized rats is linked to the generation of active expiration by mechanisms that may depend on the activation of serotonin receptors. In contrast, the decrease in body temperature induced by AIH may not require 5-HT2 receptor activation.
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spelling Acute intermittent hypoxia evokes ventilatory long-term facilitation and active expiration in unanesthetized ratsBreathing patternHypoxiaPlasticitySerotoninAcute intermittent hypoxia (AIH) modifies the functioning of the respiratory network, causing respiratory motor facilitation in anesthetized animals and a compensatory increase in pulmonary ventilation in freely behaving animals. However, it is still unclear whether the ventilatory facilitation induced by AIH in unanesthetized animals is associated with changes in the respiratory pattern. We found that Holtzman male rats (80–150 g) exposed to AIH (10 × 6% O2 for 30–40 s every 5 min, n = 9) exhibited a prolonged (30 min) increase in baseline minute ventilation (P < 0.05) compared to control animals (n = 13), combined with the occurrence of late expiratory peak flow events, suggesting the presence of active expiration. The increase in ventilation after AIH was also accompanied by reductions in arterial CO2 and body temperature (n = 5–6, P < 0.05). The systemic treatment with ketanserin (a 5-HT2 receptor antagonist) before AIH prevented the changes in ventilation and active expiration (n = 11) but potentiated the hypothermic response (n = 5, P < 0.05) when compared to appropriate control rats (n = 13). Our findings indicate that the ventilatory long-term facilitation elicited by AIH exposure in unanesthetized rats is linked to the generation of active expiration by mechanisms that may depend on the activation of serotonin receptors. In contrast, the decrease in body temperature induced by AIH may not require 5-HT2 receptor activation.Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Department of Physiology and Pathology School of Dentistry of Araraquara São Paulo State University (UNESP)Department of Physiology and Pathology School of Dentistry of Araraquara São Paulo State University (UNESP)CAPES: 001CNPq: 132363/2018-6FAPESP: 2013/17251-6FAPESP: 2018/21000-2CNPq: 310331/2017-0CNPq: 408950/2018-8CAPES: 88887.194785/2018-00Universidade Estadual Paulista (UNESP)Mendonça-Junior, Bolival A. [UNESP]V. Fernandes, Marcos [UNESP]Zoccal, Daniel B. [UNESP]2022-04-29T08:31:26Z2022-04-29T08:31:26Z2021-12-01info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articlehttp://dx.doi.org/10.1016/j.resp.2021.103768Respiratory Physiology and Neurobiology, v. 294.1878-15191569-9048http://hdl.handle.net/11449/22925410.1016/j.resp.2021.1037682-s2.0-85111727458Scopusreponame:Repositório Institucional da UNESPinstname:Universidade Estadual Paulista (UNESP)instacron:UNESPengRespiratory Physiology and Neurobiologyinfo:eu-repo/semantics/openAccess2024-09-27T14:05:43Zoai:repositorio.unesp.br:11449/229254Repositório InstitucionalPUBhttp://repositorio.unesp.br/oai/requestrepositoriounesp@unesp.bropendoar:29462024-09-27T14:05:43Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)false
dc.title.none.fl_str_mv Acute intermittent hypoxia evokes ventilatory long-term facilitation and active expiration in unanesthetized rats
title Acute intermittent hypoxia evokes ventilatory long-term facilitation and active expiration in unanesthetized rats
spellingShingle Acute intermittent hypoxia evokes ventilatory long-term facilitation and active expiration in unanesthetized rats
Mendonça-Junior, Bolival A. [UNESP]
Breathing pattern
Hypoxia
Plasticity
Serotonin
title_short Acute intermittent hypoxia evokes ventilatory long-term facilitation and active expiration in unanesthetized rats
title_full Acute intermittent hypoxia evokes ventilatory long-term facilitation and active expiration in unanesthetized rats
title_fullStr Acute intermittent hypoxia evokes ventilatory long-term facilitation and active expiration in unanesthetized rats
title_full_unstemmed Acute intermittent hypoxia evokes ventilatory long-term facilitation and active expiration in unanesthetized rats
title_sort Acute intermittent hypoxia evokes ventilatory long-term facilitation and active expiration in unanesthetized rats
author Mendonça-Junior, Bolival A. [UNESP]
author_facet Mendonça-Junior, Bolival A. [UNESP]
V. Fernandes, Marcos [UNESP]
Zoccal, Daniel B. [UNESP]
author_role author
author2 V. Fernandes, Marcos [UNESP]
Zoccal, Daniel B. [UNESP]
author2_role author
author
dc.contributor.none.fl_str_mv Universidade Estadual Paulista (UNESP)
dc.contributor.author.fl_str_mv Mendonça-Junior, Bolival A. [UNESP]
V. Fernandes, Marcos [UNESP]
Zoccal, Daniel B. [UNESP]
dc.subject.por.fl_str_mv Breathing pattern
Hypoxia
Plasticity
Serotonin
topic Breathing pattern
Hypoxia
Plasticity
Serotonin
description Acute intermittent hypoxia (AIH) modifies the functioning of the respiratory network, causing respiratory motor facilitation in anesthetized animals and a compensatory increase in pulmonary ventilation in freely behaving animals. However, it is still unclear whether the ventilatory facilitation induced by AIH in unanesthetized animals is associated with changes in the respiratory pattern. We found that Holtzman male rats (80–150 g) exposed to AIH (10 × 6% O2 for 30–40 s every 5 min, n = 9) exhibited a prolonged (30 min) increase in baseline minute ventilation (P < 0.05) compared to control animals (n = 13), combined with the occurrence of late expiratory peak flow events, suggesting the presence of active expiration. The increase in ventilation after AIH was also accompanied by reductions in arterial CO2 and body temperature (n = 5–6, P < 0.05). The systemic treatment with ketanserin (a 5-HT2 receptor antagonist) before AIH prevented the changes in ventilation and active expiration (n = 11) but potentiated the hypothermic response (n = 5, P < 0.05) when compared to appropriate control rats (n = 13). Our findings indicate that the ventilatory long-term facilitation elicited by AIH exposure in unanesthetized rats is linked to the generation of active expiration by mechanisms that may depend on the activation of serotonin receptors. In contrast, the decrease in body temperature induced by AIH may not require 5-HT2 receptor activation.
publishDate 2021
dc.date.none.fl_str_mv 2021-12-01
2022-04-29T08:31:26Z
2022-04-29T08:31:26Z
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv http://dx.doi.org/10.1016/j.resp.2021.103768
Respiratory Physiology and Neurobiology, v. 294.
1878-1519
1569-9048
http://hdl.handle.net/11449/229254
10.1016/j.resp.2021.103768
2-s2.0-85111727458
url http://dx.doi.org/10.1016/j.resp.2021.103768
http://hdl.handle.net/11449/229254
identifier_str_mv Respiratory Physiology and Neurobiology, v. 294.
1878-1519
1569-9048
10.1016/j.resp.2021.103768
2-s2.0-85111727458
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv Respiratory Physiology and Neurobiology
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.source.none.fl_str_mv Scopus
reponame:Repositório Institucional da UNESP
instname:Universidade Estadual Paulista (UNESP)
instacron:UNESP
instname_str Universidade Estadual Paulista (UNESP)
instacron_str UNESP
institution UNESP
reponame_str Repositório Institucional da UNESP
collection Repositório Institucional da UNESP
repository.name.fl_str_mv Repositório Institucional da UNESP - Universidade Estadual Paulista (UNESP)
repository.mail.fl_str_mv repositoriounesp@unesp.br
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