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Tobacco smoke-induced left ventricular remodelling is not associated with metalloproteinase-2 or -9 activation

dc.contributor.authorCastardeli, Edson
dc.contributor.authorDuarte, Daniella R.
dc.contributor.authorMinicucci, Marcos Ferreira [UNESP]
dc.contributor.authorGaiolla, Paula Schmidt Azevedo [UNESP]
dc.contributor.authorMatsubara, Beatriz Bojikian [UNESP]
dc.contributor.authorMatsubara, Luiz Shiguero [UNESP]
dc.contributor.authorCampana, Alvaro O.
dc.contributor.authorPaiva, Sergio Alberto Rupp de [UNESP]
dc.contributor.authorZornoff, Leonardo Antonio Mamede [UNESP]
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2014-05-20T13:32:52Z
dc.date.available2014-05-20T13:32:52Z
dc.date.issued2007-11-01
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.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.format.extent1081-1085
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.doi10.1016/j.ejheart.2007.09.004
dc.identifier.issn1388-9842
dc.identifier.lattes6990977122340795
dc.identifier.lattes6309835137998766
dc.identifier.lattes5016839015394547
dc.identifier.lattes1213140801402647
dc.identifier.lattes7438704034471673
dc.identifier.orcid0000-0002-5843-6232
dc.identifier.urihttp://hdl.handle.net/11449/11227
dc.identifier.wosWOS:000251484500002
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofEuropean Journal of Heart Failure
dc.relation.ispartofjcr10.683
dc.relation.ispartofsjr5,784
dc.rights.accessRightsAcesso restrito
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.typeArtigo
dcterms.licensehttp://olabout.wiley.com/WileyCDA/Section/id-406071.html
dcterms.rightsHolderElsevier B.V.
dspace.entity.typePublication
unesp.author.lattes6990977122340795
unesp.author.lattes6309835137998766
unesp.author.lattes1213140801402647[4]
unesp.author.lattes7438704034471673
unesp.author.orcid0000-0002-5843-6232[4]
unesp.campusUniversidade Estadual Paulista (UNESP), Faculdade de Medicina, Botucatupt
unesp.departmentClínica Médica - FMBpt

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