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dc.contributor.authorOkoshi, Katashi [UNESP]
dc.contributor.authorOkoshi, Marina Politi [UNESP]
dc.contributor.authorMatsubara, Beatriz Bojikian [UNESP]
dc.contributor.authorGonçalves, Giancarlo [UNESP]
dc.contributor.authorBarros, Reginaldo [UNESP]
dc.contributor.authorCicogna, Antonio Carlos [UNESP]
dc.date.accessioned2014-05-27T11:20:33Z
dc.date.available2014-05-27T11:20:33Z
dc.date.issued2002-12-01
dc.identifier.citationJournal of Medicine, v. 33, n. 5-6, p. 297-307, 2002.
dc.identifier.issn0025-7850
dc.identifier.urihttp://hdl.handle.net/11449/67064
dc.description.abstractThere still controversy about the relation between changes in myocardial contractile function and global left ventricular (LV) performance during stable concentric hypertrophy. To clarify this, we analyzed LV function in vivo and myocardial mechanics in vitro in rats with pressure overload-induced cardiac hypertrophy. Male Wistar rats (70 g) underwent ascending aorta stenosis for 8 weeks (group AAS, n=9). LV performance was assessed by transthoracic echocardiography under light anesthesia. Myocardial function was studied in isolated papillary muscle preparation during isometric contraction. The data were compared with age- and sex-matched sham-operated rats (group C, n=9). LV weight-to-body weight ratio (C: 2.0 ± 0.5 mg/g; AAS: 3.3 ± 0.7 mg/g), LV relative wall thickness (C: 0.19 ± 0.02; AAS; 0.34 ± 0.10), and LV fractional shortening (C: 54 ± 5%; AAS: 70 ± 8%) were increased in the group AAS (p<0.05). Echocardiographic analysis also indicated a significant association (r=0.74; p<0.001) between percent fractional shortening and LV relative wall thickness. The performance of AAS isolated muscle revealed that active tension (C: 6.6 ± 1.7 g/mm 2; AAS: 6.5 ± 1.5 g/mm 2) and maximum rate of tension development (C: 69 ± 21 g/mm 2/s; AAS: 69 ± 18 g/mm 2) were not significantly different from group C (p>0.05). In conclusion: 1) Compensated pressure-overload myocardial hypertrophy is associated with preserved myocardial function and increased ventricular performance; 2) The improved LV function might be due to the ventricular remodeling characterized by an increased relative wall thickness. Copyright © 2002 By PJD Publications Limited.en
dc.format.extent297-307
dc.language.isoeng
dc.relation.ispartofJournal of Medicine
dc.sourceScopus
dc.subjectAortic stenosis
dc.subjectCardiac function
dc.subjectEchocardiography
dc.subjectLeft ventricular hypertrophy
dc.subjectPapillary muscle
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectaorta stenosis
dc.subjectbody weight
dc.subjectcontrolled study
dc.subjectechocardiography
dc.subjectheart left ventricle ejection fraction
dc.subjectheart left ventricle hypertrophy
dc.subjectheart papillary muscle
dc.subjectheart rate
dc.subjectheart weight
dc.subjectmale
dc.subjectmuscle isometric contraction
dc.subjectnonhuman
dc.subjectrat
dc.subjectspontaneously hypertensive rat
dc.subjectstatistical analysis
dc.titleImproved systolic ventricular function with normal myocardial mechanics in compensated cardiac hypertrophyen
dc.typeArtigo
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.description.affiliationDepartamento de Clínica Médica Faculdade de Medicina de Botucatu UNESP, Rubião Júnior, S/N, CEP 18618 000 Botucatu, SP
dc.description.affiliationUnespDepartamento de Clínica Médica Faculdade de Medicina de Botucatu UNESP, Rubião Júnior, S/N, CEP 18618 000 Botucatu, SP
dc.identifier.doi10.1536/jhj.45.647
dc.rights.accessRightsAcesso aberto
dc.identifier.scopus2-s2.0-34648816391
unesp.campusUniversidade Estadual Paulista (Unesp), Faculdade de Medicina, Botucatupt
dc.identifier.file2-s2.0-34648816391.pdf
dc.identifier.lattes1590971576309420
dc.identifier.lattes4463138671998432
dc.identifier.lattes6990977122340795
dc.identifier.lattes9418970103564137
unesp.author.lattes1590971576309420
unesp.author.lattes4463138671998432
unesp.author.lattes6990977122340795
unesp.author.lattes9418970103564137[6]
unesp.author.orcid0000-0002-4402-6523[6]
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