BRAINSTEM AREAS ACTIVATED BY INTERMITTENT APNEA in AWAKE UNRESTRAINED RATS

dc.contributor.authorFerreira, C. B. [UNIFESP]
dc.contributor.authorSchoorlemmer, G. H. [UNIFESP]
dc.contributor.authorRossi, M. V. [UNIFESP]
dc.contributor.authorTakakura, A. C.
dc.contributor.authorBarna, B. F.
dc.contributor.authorMoreira, T. S.
dc.contributor.authorCravo, S. L. [UNIFESP]
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.date.accessioned2016-01-24T14:40:35Z
dc.date.available2016-01-24T14:40:35Z
dc.date.issued2015-06-25
dc.description.abstractWe investigated the role of the autonomic nervous system to cardiovascular responses to obstructive apnea in awake, unrestrained rats, and measured expression of Fos induced by apnea in the brainstem. We implanted a tracheal balloon contained in a rigid tube to allow the induction of apnea without inducing pain in the trachea. During bouts of 15 s of apnea, heart rate fell from 371 +/- 8 to 161 +/- 11 bpm (mean +/- SEM, n = 15, p < 0.01) and arterial pressure increased from 115 +/- 2 to 131 +/- 4 mmHg (p < 0.01). Bradycardia was due to parasympathetic activity because it was blocked by the muscarinic antagonist, methylatropine. the pressor response was due to vasoconstriction caused by sympathetic activation because it was blocked by the alpha(1) antagonist, prazosin. Apnea induced Fos expression in several brainstem areas involved in cardiorespiratory control such as the nucleus of the solitary tract (NTS), ventrolateral medulla (VLM), and pons. Ligation of the carotid body artery reduced apnea-induced bradycardia, blocked heart rate responses to i.v. injection of cyanide, reduced Fos expression in the caudal NTS, and increased Fos expression in the rostral VLM. in conclusion, apnea activates neurons in regions that process signals from baroreceptors, chemoreceptors, pulmonary receptors, and regions responsible for autonomic and respiratory activity both in the presence and absence of carotid chemoreceptors. (C) 2015 IBRO. Published by Elsevier B.V. All rights reserved.en
dc.description.affiliationUniversidade Federal de São Paulo, Dept Physiol, BR-04023062 São Paulo, Brazil
dc.description.affiliationUniv São Paulo, Inst Biomed Sci, Dept Pharmacol, BR-05508000 São Paulo, Brazil
dc.description.affiliationUniv São Paulo, Inst Biomed Sci, Dept Physiol & Biophys, BR-05508000 São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Physiol, BR-04023062 São Paulo, Brazil
dc.description.sourceWeb of Science
dc.format.extent262-271
dc.identifierhttp://dx.doi.org/10.1016/j.neuroscience.2015.04.007
dc.identifier.citationNeuroscience. Oxford: Pergamon-Elsevier B.V., v. 297, p. 262-271, 2015.
dc.identifier.doi10.1016/j.neuroscience.2015.04.007
dc.identifier.issn0306-4522
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/39144
dc.identifier.wosWOS:000354177900025
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofNeuroscience
dc.rightsAcesso restrito
dc.rights.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.subjectobstructive apneaen
dc.subjectarterial chemoreceptorsen
dc.subjectcFos immunoreactivityen
dc.subjectmedulla oblongataen
dc.subjecthypoxiaen
dc.titleBRAINSTEM AREAS ACTIVATED BY INTERMITTENT APNEA in AWAKE UNRESTRAINED RATSen
dc.typeArtigo
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