Myocardial dysfunction induced by food restriction is related to morphological damage in normotensive middle-aged rats

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dc.contributor.authorSugizaki, M.
dc.contributor.authorCarvalho, R. F.
dc.contributor.authorAragon, F. F.
dc.contributor.authorPadovani, Carlos Roberto [UNESP]
dc.contributor.authorOkoshi, Katashi [UNESP]
dc.contributor.authorOkoshi, Marina Politi [UNESP]
dc.contributor.authorZanati, S. G.
dc.contributor.authorDal Pai-Silva, M.
dc.contributor.authorNovelli, ELB
dc.contributor.authorCicogna, Antonio Carlos [UNESP]
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2014-05-20T13:47:41Z
dc.date.available2014-05-20T13:47:41Z
dc.date.issued2005-07-01
dc.description.abstractPrevious works from our laboratory have revealed that food restriction (FR) promotes discrete myocardial dysfunction in young rats. We examined the effects of FR on cardiac function, in vivo and in vitro, and ultrastructural changes in the heart of middle-aged rats. Twelve-month-old Wistar- Kyoto rats were fed a control (C) or restricted diet (daily intake reduced to 50% of the control group) for 90 days. Cardiac performance was studied by echocardiogram and in isolated left ventricular (LV) papillary muscle by isometric contraction in basal condition, after calcium chloride (5.2 mM) and beta- adrenergic stimulation with isoproterenol (10(-6) M). FR did not change left ventricular function, but increased time to peak tension, and decreased maximum rate of papillary muscle tension development. Inotropic maneuvers promoted similar effects in both groups. Ultrastructural alterations were seen in most FR rat muscle fibers and included, absence and/or disorganization of myofilaments and Z line, hyper-contracted myofibrils, polymorphic and swollen mitochondria with disorganized cristae, and a great quantity of collagen fibrils. In conclusion, cardiac muscle sensitivity to isoproterenol and elevation of extracellular calcium concentration is preserved in middle-aged FR rats. The intrinsic muscle performance depression might be related to morphological damage.en
dc.description.affiliationUniv Estadual Paulista Julio Mesquita Filho, Fac Med Botucatu, Sch Med, Dept Internal Med, BR-18618000 Botucatu, SP, Brazil
dc.description.affiliationUniv Estadual Paulista Julio Mesquita Filho, State Univ Julio Mesquita Filho, Dept Biochem, BR-18618000 Botucatu, SP, Brazil
dc.description.affiliationUniv Estadual Paulista Julio Mesquita Filho, State Univ Julio Mesquita Filho, Dept Morphol, BR-18618000 Botucatu, SP, Brazil
dc.description.affiliationUniv Estadual Paulista Julio Mesquita Filho, State Univ Julio Mesquita Filho, Dept Biostat, BR-18618000 Botucatu, SP, Brazil
dc.description.affiliationUnespUniv Estadual Paulista Julio Mesquita Filho, Fac Med Botucatu, Sch Med, Dept Internal Med, BR-18618000 Botucatu, SP, Brazil
dc.description.affiliationUnespUniv Estadual Paulista Julio Mesquita Filho, State Univ Julio Mesquita Filho, Dept Biochem, BR-18618000 Botucatu, SP, Brazil
dc.description.affiliationUnespUniv Estadual Paulista Julio Mesquita Filho, State Univ Julio Mesquita Filho, Dept Morphol, BR-18618000 Botucatu, SP, Brazil
dc.description.affiliationUnespUniv Estadual Paulista Julio Mesquita Filho, State Univ Julio Mesquita Filho, Dept Biostat, BR-18618000 Botucatu, SP, Brazil
dc.format.extent641-649
dc.identifierhttp://dx.doi.org/10.1007/s11373-005-7652-y
dc.identifier.citationJournal of Biomedical Science. Dordrecht: Springer, v. 12, n. 4, p. 641-649, 2005.
dc.identifier.doi10.1007/s11373-005-7652-y
dc.identifier.issn1021-7770
dc.identifier.lattes5406518799128485
dc.identifier.lattes9418970103564137
dc.identifier.lattes8727897080522289
dc.identifier.lattes4463138671998432
dc.identifier.lattes1590971576309420
dc.identifier.lattes4125344753100454
dc.identifier.orcid0000-0003-1270-7372
dc.identifier.urihttp://hdl.handle.net/11449/16983
dc.identifier.wosWOS:000233371300007
dc.language.isoeng
dc.publisherSpringer
dc.relation.ispartofJournal of Biomedical Science
dc.relation.ispartofjcr3.466
dc.relation.ispartofsjr1,302
dc.rights.accessRightsAcesso restrito
dc.sourceWeb of Science
dc.subjectfood restrictionpt
dc.subjectmyocardial ultrastructurept
dc.subjectpapillary musclept
dc.subjectratpt
dc.subjectventricular functionpt
dc.titleMyocardial dysfunction induced by food restriction is related to morphological damage in normotensive middle-aged ratsen
dc.typeArtigo
dcterms.licensehttp://www.springer.com/open+access/authors+rights?SGWID=0-176704-12-683201-0
dcterms.rightsHolderSpringer
unesp.author.lattes5406518799128485
unesp.author.lattes9418970103564137[10]
unesp.author.lattes8727897080522289[4]
unesp.author.lattes4463138671998432
unesp.author.lattes1590971576309420
unesp.author.lattes4125344753100454[2]
unesp.author.orcid0000-0002-0607-8189[7]
unesp.author.orcid0000-0002-4402-6523[10]
unesp.author.orcid0000-0002-7719-9682[4]
unesp.author.orcid0000-0003-1270-7372[2]
unesp.campusUniversidade Estadual Paulista (Unesp), Instituto de Biociências, Botucatupt
unesp.campusUniversidade Estadual Paulista (Unesp), Faculdade de Medicina, Botucatupt

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