Inducible Nitric Oxide Synthase Inhibition Attenuates Physical Stress-Induced Lung Hyper-Responsiveness and Oxidative Stress in Animals with Lung Inflammation

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dc.contributor.authorMarques, Ricardo Henrique
dc.contributor.authorReis, Fabiana Gomes
dc.contributor.authorStarling, Claudia Miranda
dc.contributor.authorCabido, Claudia
dc.contributor.authorAlmeida-Reis, Rafael de
dc.contributor.authorDohlnikoff, Marisa
dc.contributor.authorPrado, Carla Máximo [UNIFESP]
dc.contributor.authorLeick, Edna Aparecida
dc.contributor.authorMartins, Milton de Arruda
dc.contributor.authorTiberio, Iolanda de Fátima Lopes Calvo
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionUniv Mogi das Cruzes
dc.date.accessioned2016-01-24T14:17:46Z
dc.date.available2016-01-24T14:17:46Z
dc.date.issued2012-01-01
dc.description.abstractMechanisms involved in stress-induced asthmatic alterations have been poorly characterised. We assessed whether inducible nitric oxide synthase (iNOS) inhibition modulates the stress-amplified lung parenchyma responsiveness, oxidative stress and extracellular matrix remodelling that was previously increased by chronic lung inflammation. Guinea pigs were subjected to 7 exposures to ovalbumin (1-5 mg/ml) or saline (OVA and SAL groups) over 4 weeks. To induce behavioural stress, animals were subjected to a forced swimming protocol (5 times/week, over 2 weeks; SAL-Stress and OVA-Stress groups) 24 h after the 4th inhalation. 1400W (iNOS-specific inhibitor) was administered intraperitoneally in the last 4 days of the protocol (SAL-1400W, OVA-1400W, SAL-Stress+1400W and OVA-Stress+1400W groups). Seventy-two hours after the last inhalation, animals were anaesthetised and exsanguinated, and adrenal glands were removed. Lung tissue resistance and elastance were evaluated by oscillatory mechanics and submitted for histopathological evaluation. Stressed animals had higher adrenal weights compared to non-stressed groups, which were reduced by 1400W treatment. Behavioural stress in sensitised animals amplified the resistance and elastance responses after antigen challenge, numbers of eosinophils and iNOS+ cells, actin content and 8-iso-PGF2 alpha density in the distal lung compared to the OVA group. 1400W treatment in ovalbumin-exposed and stressed animals reduced lung mechanics, iNOS+ cell numbers and 8-iso-PGF2a density compared to sensitised and stressed animals that received vehicle treatment. We concluded that stress amplifies the distal lung constriction, eosinophilic inflammation, iNOS expression, actin content and oxidative stress previously induced by chronic lung inflammation. iNOS-derived NO contributes to stress-augmented lung tissue functional alterations in this animal model and is at least partially due to activation of the oxidative stress pathway. copyright (C) 2012S. Karger AG, Baselen
dc.description.affiliationUniv São Paulo, Fac Med, Dept Clin Med, BR-01246903 São Paulo, Brazil
dc.description.affiliationUniv São Paulo, Fac Med, Dept Patol, BR-01246903 São Paulo, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Dept Ciencias Biol, Diadema, Brazil
dc.description.affiliationUniv Mogi das Cruzes, Nucleo Pesquisas Tecnol, Mogi Das Cruzes, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Ciencias Biol, Diadema, Brazil
dc.description.sourceWeb of Science
dc.format.extent158-170
dc.identifierhttps://dx.doi.org/10.1159/000331264
dc.identifier.citationNeuroimmunomodulation. Basel: Karger, v. 19, n. 3, p. 158-170, 2012.
dc.identifier.doi10.1159/000331264
dc.identifier.issn1021-7401
dc.identifier.urihttps://repositorio.unifesp.br/handle/11600/34494
dc.identifier.wosWOS:000301330800005
dc.language.isoeng
dc.publisherKarger
dc.relation.ispartofNeuroimmunomodulation
dc.rightsinfo:eu-repo/semantics/restrictedAccess
dc.rights.licensehttp://www.karger.com/Services/RightsPermissions
dc.subjectExperimental asthma modelen
dc.subjectBehavioural stressen
dc.subjectLung parenchymaen
dc.subjectInducible nitric oxide synthaseen
dc.subjectOxidative stressen
dc.titleInducible Nitric Oxide Synthase Inhibition Attenuates Physical Stress-Induced Lung Hyper-Responsiveness and Oxidative Stress in Animals with Lung Inflammationen
dc.typeinfo:eu-repo/semantics/article
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