Publicação:
Tissue Vitamin A Insufficiency Results in Adverse Ventricular Remodeling after Experimental Myocardial Infarction

dc.contributor.authorMinicucci, Marcos Ferreira [UNESP]
dc.contributor.authorGaiolla, Paula Schmidt Azevedo [UNESP]
dc.contributor.authorOliveira, Silvio A.
dc.contributor.authorMartinez, Paula F.
dc.contributor.authorChiuso-Minicucci, Fernanda [UNESP]
dc.contributor.authorPolegato, Bertha Furlan [UNESP]
dc.contributor.authorJustulin, Luis A. [UNESP]
dc.contributor.authorMatsubara, Luiz Shiguero [UNESP]
dc.contributor.authorMatsubara, Beatriz Bojikian [UNESP]
dc.contributor.authorPaiva, Sergio Alberto Rupp de [UNESP]
dc.contributor.authorZornoff, Leonardo Antonio Mamede [UNESP]
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2014-05-20T13:51:13Z
dc.date.available2014-05-20T13:51:13Z
dc.date.issued2010-01-01
dc.description.abstractBackground/Aims: The role of tissue vitamin-A insufficiency on post-infarction ventricular remodeling is unknown. We tested the hypothesis that cardiac vitamin A insufficiency on post-infarction is associated with adverse myocardial remodeling. Methods: After infarction, rats were allocated into two groups: C (controls, n=25); VA (dietary vitamin A restriction, n= 26). After 3 months, the animals were submitted to echocardiogram, morphometric and biochemical analysis. Results: Rats fed the vitamin-A-deficient diet had lower heart and liver retinol concentration and normal plasma retinol. There were no differences in infarct size between the groups. VA showed higher diastolic left ventricular area normalised by body weight (C= 1.81 +/- 0.4 cm2/kg, VA= 2.15 +/- 0.3 cm2/kg; p=0.03), left ventricular diameter (C= 9.4 +/- 1.4 mm, VA= 10.5 +/- 1.2 mm; p=0.04), but similar systolic ventricular fractional area change (C= 33.0 +/- 10.0 %, VA= 32.1 +/- 8.7 %; p=0.82). VA showed decreased isovolumetric relaxation time normalised by heart rate (C= 68.8 +/- 11.4 ms, VA= 56.3 +/- 16.8 ms; p=0.04). VA showed higher interstitial collagen fraction (C= 2.8 +/- 0.9 %, VA= 3.7 +/- 1.1 %; p=0.05). There were no differences in myosin heavy chain expression, metalloproteinase 2 and 9 activation, or IFN-gamma and TNF-alpha cardiac levels. Conclusion: Local tissue vitamin A insufficiency intensified ventricular remodeling after MI, worsening diastolic dysfunction. Copyright (C) 2010 S. Karger AG, Baselen
dc.description.affiliationSão Paulo State Univ, Dept Internal Med, Botucatu Med Sch, UNESP,Fac Med Botucatu, BR-18618000 Botucatu, SP, Brazil
dc.description.affiliationSão Paulo State Univ, Dept Microbiol & Immunol, Inst Biosci, BR-18618000 Botucatu, SP, Brazil
dc.description.affiliationSão Paulo State Univ, Dept Morphol, Inst Biosci, BR-18618000 Botucatu, SP, Brazil
dc.description.affiliationUnespSão Paulo State Univ, Dept Internal Med, Botucatu Med Sch, UNESP,Fac Med Botucatu, BR-18618000 Botucatu, SP, Brazil
dc.description.affiliationUnespSão Paulo State Univ, Dept Microbiol & Immunol, Inst Biosci, BR-18618000 Botucatu, SP, Brazil
dc.description.affiliationUnespSão Paulo State Univ, Dept Morphol, Inst Biosci, BR-18618000 Botucatu, SP, Brazil
dc.format.extent523-530
dc.identifierhttp://dx.doi.org/10.1159/000322320
dc.identifier.citationCellular Physiology and Biochemistry. Basel: Karger, v. 26, n. 4-5, p. 523-530, 2010.
dc.identifier.doi10.1159/000322320
dc.identifier.fileWOS000283859000004.pdf
dc.identifier.issn1015-8987
dc.identifier.lattes6309835137998766
dc.identifier.lattes6990977122340795
dc.identifier.lattes5016839015394547
dc.identifier.lattes1213140801402647
dc.identifier.orcid0000-0002-5843-6232
dc.identifier.urihttp://hdl.handle.net/11449/18285
dc.identifier.wosWOS:000283859000004
dc.language.isoeng
dc.publisherKarger
dc.relation.ispartofCellular Physiology and Biochemistry
dc.relation.ispartofjcr5.500
dc.relation.ispartofsjr1,561
dc.rights.accessRightsAcesso aberto
dc.sourceWeb of Science
dc.subjectVentricular functionen
dc.subjectFibrosisen
dc.subjectVentricular dilatationen
dc.titleTissue Vitamin A Insufficiency Results in Adverse Ventricular Remodeling after Experimental Myocardial Infarctionen
dc.typeArtigo
dcterms.licensehttp://www.karger.com/Services/OpenAccessLicense
dcterms.rightsHolderKarger
dspace.entity.typePublication
unesp.author.lattes6309835137998766
unesp.author.lattes6990977122340795
unesp.author.lattes1213140801402647[2]
unesp.author.lattes4563764623232492[6]
unesp.author.orcid0000-0002-2875-9532[6]
unesp.author.orcid0000-0003-4412-1990[10]
unesp.author.orcid0000-0002-5980-4367[1]
unesp.author.orcid0000-0002-8895-9456[3]
unesp.author.orcid0000-0002-5843-6232[2]
unesp.campusUniversidade Estadual Paulista (Unesp), Instituto de Biociências, Botucatupt
unesp.campusUniversidade Estadual Paulista (Unesp), Faculdade de Medicina, Botucatupt
unesp.departmentClínica Médica - FMBpt
unesp.departmentMicrobiologia e Imunologia - IBBpt
unesp.departmentMorfologia - IBBpt

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