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dc.contributor.authorCastardeli, Edson-
dc.contributor.authorDuarte, Daniella R.-
dc.contributor.authorMinicucci, Marcos Ferreira-
dc.contributor.authorGaiolla, Paula Schmidt Azevedo-
dc.contributor.authorMatsubara, Beatriz Bojikian-
dc.contributor.authorMatsubara, Luiz Shiguero-
dc.contributor.authorCampana, Alvaro O.-
dc.contributor.authorPaiva, Sergio Alberto Rupp de-
dc.contributor.authorZornoff, Leonardo Antonio Mamede-
dc.date.accessioned2014-05-20T13:32:52Z-
dc.date.accessioned2016-10-25T16:51:05Z-
dc.date.available2014-05-20T13:32:52Z-
dc.date.available2016-10-25T16:51:05Z-
dc.date.issued2007-11-01-
dc.identifierhttp://dx.doi.org/10.1016/j.ejheart.2007.09.004-
dc.identifier.citationEuropean Journal of Heart Failure. Amsterdam: Elsevier B.V., v. 9, n. 11, p. 1081-1085, 2007.-
dc.identifier.issn1388-9842-
dc.identifier.urihttp://hdl.handle.net/11449/11227-
dc.identifier.urihttp://acervodigital.unesp.br/handle/11449/11227-
dc.description.abstractAim: To investigate the role of MMP-2 and MMP-9 in cardiac remodelling induced by tobacco smoke exposure in rats.Methods: Rats were allocated into two groups: C (n = 9): control animals; ETS (n = 9): exposed to tobacco smoke. After 4months, the animals underwent echocardiography, morphometric study and determination of MMP-2 and MMP-9 activity.Results: ETS rats had larger diastolic (C= 15.6 +/- 1.2 mm/kg, ETS = 18.0 +/- 0.9 mm/kg; p < 0.001) and systolic (C= 7.3 +/- 1.2 mm/kg, ETS = 9.2 0.9 mm/kg; p = 0.001) ventricular diameters adjusted for body weight. Fractional shortening (C= 53 +/- 4.8%, ETS = 48 +/- 3.3%; p = 0.031) and ejection fraction (C= 0. 89 +/- 0.03 5 ETS = 0. 86 +/- 0.02; p = 0.03 0) were smaller in the ETS group. Myocyte cross-sectional area (C= 245 8 mu m(2), ETS=253 8 mu m(2); p = 0.028) was higher in ETS rats. There were no differences in MNtP-2 (C=50 +/- 14%; ETS 43 +/- 11%, p 0.22 +/- 8) or MMP-9 (C=0.36 +/- 0.3%; ETS=0.62 +/- 0.3%, p=0.630) activity between the groups.Conclusion: MMP-2 and MMP-9 did not participate in the remodelling process induced by tobacco smoke exposure. (c) 2007 European Society of Cardiology. Published by Elsevier B.V. All rights reserved.en
dc.format.extent1081-1085-
dc.language.isoeng-
dc.publisherElsevier B.V.-
dc.sourceWeb of Science-
dc.subjectventricular functionpt
dc.subjectcardiac remodellingpt
dc.subjectventricular dilatationpt
dc.titleTobacco smoke-induced left ventricular remodelling is not associated with metalloproteinase-2 or -9 activationen
dc.typeoutro-
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)-
dc.description.affiliationUNESP, São Paulo State Univ, Fac Med Botucatu, Dept Clin Med, BR-18618000 Botucatu, SP, Brazil-
dc.description.affiliationUnespUNESP, São Paulo State Univ, Fac Med Botucatu, Dept Clin Med, BR-18618000 Botucatu, SP, Brazil-
dc.identifier.doi10.1016/j.ejheart.2007.09.004-
dc.identifier.wosWOS:000251484500002-
dc.rights.accessRightsAcesso restrito-
dc.relation.ispartofEuropean Journal of Heart Failure-
Appears in Collections:Artigos, TCCs, Teses e Dissertações da Unesp

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