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Utilize este identificador para citar ou criar um link para este item: http://acervodigital.unesp.br/handle/11449/8355
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dc.contributor.authorde Oliveira Cavalcanti, Renato Albuquerque-
dc.contributor.authorda Pureza, Demilto Yamaguchi-
dc.contributor.authorde Melo, Mariana Pereira-
dc.contributor.authorde Souza, Romeu Rodrigues-
dc.contributor.authorBergamaschi, Cassia T.-
dc.contributor.authorAmaral, Sandra Lia do-
dc.contributor.authorTang, Helen-
dc.contributor.authorLoesch, Andrzej-
dc.contributor.authorCoppi Maciel Ribeiro, Antonio Augusto-
dc.date.accessioned2014-05-20T13:26:06Z-
dc.date.accessioned2016-10-25T16:46:18Z-
dc.date.available2014-05-20T13:26:06Z-
dc.date.available2016-10-25T16:46:18Z-
dc.date.issued2009-05-01-
dc.identifierhttp://dx.doi.org/10.1002/jnr.21961-
dc.identifier.citationJournal of Neuroscience Research. Hoboken: Wiley-liss, v. 87, n. 6, p. 1334-1342, 2009.-
dc.identifier.issn0360-4012-
dc.identifier.urihttp://hdl.handle.net/11449/8355-
dc.identifier.urihttp://acervodigital.unesp.br/handle/11449/8355-
dc.description.abstractStellate ganglion (SG) represents the main sympathetic input to the heart. This study aimed at investigating physical exercise-related changes in the quantitative aspects of SG neurons in treadmill-exercised Wistar rats. By applying state-of-the-art design-based stereology, the SG volume, total number of SG neurons, mean perikaryal volume of SG neurons, and the total volume of neurons in the whole SG have been examined. Arterial pressure and heart rate were also measured at the end of the exercise period. The present study showed that a low-intensity exercise training program caused a 12% decrease in the heart rate of trained rats. In contrast, there were no effects on systolic pressure, diastolic pressure, or mean arterial pressure. As to quantitative changes related to physical exercise, the main findings were a 21% increase in the fractional volume occupied by neurons in the SG, and an 83% increase in the mean perikaryal volume of SG neurons in treadmill-trained rats, which shows a remarkable neuron hypertrophy. It seems reasonable to infer that neuron hypertrophy may have been the result of a functional overload imposed on the SG neurons by initial posttraining sympathetic activation. From the novel stereological data we provide, further investigations are needed to shed light on the mechanistic aspect of neuron hypertrophy: what role does neuron hypertrophy play? Could neuron hypertrophy be assigned to the functional overload induced by physical exercise? (C) 2008 Wiley-Liss, Inc.en
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)-
dc.format.extent1334-1342-
dc.language.isoeng-
dc.publisherWiley-liss-
dc.sourceWeb of Science-
dc.subjectstereologyen
dc.subjectextrinsic cardiac innervationen
dc.subjectphysical exerciseen
dc.subjectstellate ganglionen
dc.subjectratsen
dc.titleLow-intensity Treadmill Exercise-related Changes in the Rat Stellate Ganglion Neuronsen
dc.typeoutro-
dc.contributor.institutionUniversidade de São Paulo (USP)-
dc.contributor.institutionUniversidade São Judas Tadeu (USJT)-
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)-
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)-
dc.contributor.institutionUCL-
dc.description.affiliationUniv São Paulo, Fac Med Vet & Zootecnia, Dept Cirurgia, Coll Vet Med,LSSCA, BR-05508270 São Paulo, Brazil-
dc.description.affiliationUniv São Paulo, Inst Math & Stat, Dept Stat, BR-05508270 São Paulo, Brazil-
dc.description.affiliationUniversidade São Judas Tadeu (USJT), Phys Educ Postgrad Course, São Paulo, Brazil-
dc.description.affiliationUniv Fed São Paulo, Dept Biosci, Santos, Brazil-
dc.description.affiliationSão Paulo State Univ, UNESP, Fac Sci, Dept Phys Educ, Bauru, Brazil-
dc.description.affiliationUCL, Sch Med, Res Dept Inflammat, London W1N 8AA, England-
dc.description.affiliationUnespSão Paulo State Univ, UNESP, Fac Sci, Dept Phys Educ, Bauru, Brazil-
dc.description.sponsorshipIdFAPESP: 05/02411-1-
dc.identifier.doi10.1002/jnr.21961-
dc.identifier.wosWOS:000264907400006-
dc.rights.accessRightsAcesso restrito-
dc.relation.ispartofJournal of Neuroscience Research-
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