GROWTH HORMONE ATTENUATES MYOCARDIAL FIBROSIS IN RATS WITH CHRONIC PRESSURE OVERLOAD-INDUCED LEFT VENTRICULAR HYPERTROPHY

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dc.contributor.authorMoreira, Vanessa O. [UNESP]
dc.contributor.authorPereira, Camila A. [UNESP]
dc.contributor.authorSilva, Mirella O. [UNESP]
dc.contributor.authorFelisbino, Sergio L. [UNESP]
dc.contributor.authorCicogna, Antonio Carlos [UNESP]
dc.contributor.authorOkoshi, Katashi [UNESP]
dc.contributor.authorAragon, Flávio Ferrari [UNESP]
dc.contributor.authorPadovani, Carlos Roberto [UNESP]
dc.contributor.authorOkoshi, Marina Politi [UNESP]
dc.contributor.authorCastro, Ana V. B. [UNESP]
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2014-05-20T13:48:08Z
dc.date.available2014-05-20T13:48:08Z
dc.date.issued2009-03-01
dc.description.abstract1. The role of growth hormone (GH) in cardiac remodelling and function in chronic and persistent pressure overload-induced left ventricular hypertrophy has not been defined. The aim of the present study was to assess short-term GH treatment on left ventricular function and remodelling in rats with chronic pressure overload-induced hypertrophy.2. Twenty-six weeks after induction of ascending aortic stenosis (AAS), rats were treated with daily subcutaneous injections of recombinant human GH (1 mg/kg per day; AAS-GH group) or saline (AAS-P group) for 14 days. Sham-operated animals served as controls. Left ventricular function was assessed by echocardiography before and after GH treatment. Myocardial fibrosis was evaluated by histological analysis.3. Before GH treatment, AAS rats presented similar left ventricular function and structure. Treatment of rats with GH after the AAS procedure did not change bodyweight or heart weight, both of which were higher in the AAS groups than in the controls. After GH treatment, posterior wall shortening velocity (PWSV) was lower in the AAS-P group than in the control group. However, in the AAS-GH group, PWSV was between that in the control and AAS-P groups and did not differ significantly from either group. Fractional collagen (% of total area) was significantly higher in the AAS-P and AAS-GH groups compared with control (10.34 +/- 1.29, 4.44 +/- 1.37 and 1.88 +/- 0.88%, respectively; P < 0.05) and was higher still in the AAS-P group compared with the AAS-GH group.4. The present study has shown that short-term administration of GH to rats with chronic pressure overload-induced left ventricular hypertrophy induces cardioprotection by attenuating myocardial fibrosis.en
dc.description.affiliationSão Paulo State Univ, UNESP, Botucatu Med Sch, Dept Internal Med, Botucatu, SP, Brazil
dc.description.affiliationUnespSão Paulo State Univ, UNESP, Botucatu Med Sch, Dept Internal Med, Botucatu, SP, Brazil
dc.description.sponsorshipFundação para o Desenvolvimento da UNESP (FUNDUNESP)
dc.format.extent325-330
dc.identifierhttp://dx.doi.org/10.1111/j.1440-1681.2008.05086.x
dc.identifier.citationClinical and Experimental Pharmacology and Physiology. Malden: Wiley-blackwell Publishing, Inc, v. 36, n. 3, p. 325-330, 2009.
dc.identifier.doi10.1111/j.1440-1681.2008.05086.x
dc.identifier.issn0305-1870
dc.identifier.lattes9418970103564137
dc.identifier.lattes1590971576309420
dc.identifier.lattes4463138671998432
dc.identifier.urihttp://hdl.handle.net/11449/17170
dc.identifier.wosWOS:000265548900013
dc.language.isoeng
dc.publisherWiley-Blackwell Publishing, Inc
dc.relation.ispartofClinical and Experimental Pharmacology and Physiology
dc.relation.ispartofsjr0,759
dc.rights.accessRightsAcesso restrito
dc.sourceWeb of Science
dc.subjectascending aortic stenosisen
dc.subjectechocardiogramen
dc.subjectgrowth hormoneen
dc.subjectmyocardial fibrosisen
dc.subjectraten
dc.subjectventricular functionen
dc.subjectventricular hypertrophyen
dc.titleGROWTH HORMONE ATTENUATES MYOCARDIAL FIBROSIS IN RATS WITH CHRONIC PRESSURE OVERLOAD-INDUCED LEFT VENTRICULAR HYPERTROPHYen
dc.typeArtigo
dcterms.licensehttp://olabout.wiley.com/WileyCDA/Section/id-406071.html
dcterms.rightsHolderWiley-blackwell Publishing, Inc
unesp.author.lattes9418970103564137[5]
unesp.author.lattes1590971576309420
unesp.author.lattes4463138671998432
unesp.author.lattes8727897080522289[8]
unesp.author.orcid0000-0002-7719-9682[8]
unesp.author.orcid0000-0001-8980-8839[9]
unesp.author.orcid0000-0002-4402-6523[5]
unesp.campusUniversidade Estadual Paulista (Unesp), Faculdade de Medicina, Botucatupt

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