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dc.contributor.authorDe Stefano, Laercio Martins-
dc.contributor.authorMatsubara, Luiz Shiguero-
dc.contributor.authorMatsubara, Beatriz Bojikian-
dc.date.accessioned2014-05-20T13:32:51Z-
dc.date.accessioned2016-10-25T16:51:05Z-
dc.date.available2014-05-20T13:32:51Z-
dc.date.available2016-10-25T16:51:05Z-
dc.date.issued2006-12-01-
dc.identifierhttp://dx.doi.org/10.1016/j.ejheart.2006.02.005-
dc.identifier.citationEuropean Journal of Heart Failure. Amsterdam: Elsevier B.V., v. 8, n. 8, p. 784-789, 2006.-
dc.identifier.issn1388-9842-
dc.identifier.urihttp://hdl.handle.net/11449/11223-
dc.identifier.urihttp://acervodigital.unesp.br/handle/11449/11223-
dc.description.abstractThe aim this study was to evaluate systolic and diastolic function in volume overload induced myocardial hypertrophy in rats.Volume overload myocardial hypertrophy was induced in thirteen male Wistar rats by creating infrarenal arteriovenous fistula (AVF). The results were compared with a SHAM operated group (n = 11). Eight weeks after surgery, tail-cuff blood pressure was recorded, then rats were sacrificed for isolated heart studies using Langendorffs preparation.AVF rats presented increased left and right ventricular weights, compared to controls. The increased normalized ventricular volume (V0/LVW, 0.141 +/- 0.035 mL/g vs. 0.267 +/- 0.071 mL/g, P < 0.001) in the AVF group indicated chamber dilation. Myocardial hydroxyproline concentration remained unchanged. There was a significant decrease in +dP/dt (3318 +/- 352 mm Hg s(-1) vs. 2769 +/- 399 mm Hg s(-1); P=0,002), end-systolic pressure-volume relation (246 +/- 56 mm Hg mL(-1) vs. 114 +/- 63 mm Hg mL(-1);, P < 0,001), and -dP/dt (1746 +/- 240 min Hg s(-1) vs. 1361 +/- 217 mm Hg s(-1), P < 0.001) in the AVF group, which presented increased ventricular compliance (Delta V-25: SHAM=0.172 +/- 0.05 mL vs. AVF=0.321 +/- 0.072 mL, P < 0.001) with preserved myocardial passive stiffness (Strain(25): SHAM=13.5 +/- 3.0% vs. AVF=12.3 +/- 1.9%, P > 0.05).We conclude that volume-overload induced hypertrophy causes myocardial systolic and diastolic dysfunction with increased ventricular compliance. These haemodynamic features help to explain the long-term compensatory phase of chronic volume overload before transition to overt congestive heart failure. (c) 2006 European Society of Cardiology. Published by Elsevier B.V. All rights reserved.en
dc.format.extent784-789-
dc.language.isoeng-
dc.publisherElsevier B.V.-
dc.sourceWeb of Science-
dc.subjectcardiac hypertrophypt
dc.subjectventricular dilationpt
dc.subjectvolume overloadpt
dc.subjectmyocardial contractilitypt
dc.titleMyocardial dysfunction with increased ventricular compliance in volume overload hypertrophyen
dc.typeoutro-
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)-
dc.description.affiliationUNESP, Fac Med Botucatu, Dept Clin Med, Botucatu Sch Med, BR-18618000 São Paulo, Brazil-
dc.description.affiliationUnespUNESP, Fac Med Botucatu, Dept Clin Med, Botucatu Sch Med, BR-18618000 São Paulo, Brazil-
dc.identifier.doi10.1016/j.ejheart.2006.02.005-
dc.identifier.wosWOS:000243255500003-
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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