dc.contributorUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2014-05-27T11:24:46Z
dc.date.accessioned2022-10-05T18:22:07Z
dc.date.available2014-05-27T11:24:46Z
dc.date.available2022-10-05T18:22:07Z
dc.date.created2014-05-27T11:24:46Z
dc.date.issued2010-08-13
dc.identifierCase Reports and Clinical Practice Review, v. 16, n. 8, 2010.
dc.identifier1507-6164
dc.identifier1643-3742
dc.identifier1234-1010
dc.identifierhttp://hdl.handle.net/11449/71818
dc.identifierWOS:000280762400010
dc.identifier2-s2.0-77955365642
dc.identifierWOS000280762400010.pdf
dc.identifier9418970103564137
dc.identifier8727897080522289
dc.identifier4463138671998432
dc.identifier5016839015394547
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/3920946
dc.description.abstractBackground: The aim of this study was to analyze stable hypertrophied myocardial function and its response to inotropic maneuvers in rats submitted to renovascular hypertension for a 10-week period (RHT group, n=10). Material/Methods: Myocardial performance was studied in isolated left ventricle papillary muscles in isometric contraction under the following conditions: at postrest contraction of 30 seconds (PRC), at extracellular calcium (ECa 2+) chloride concentration of 1.25 and 5.20 mM, and after beta-adrenergic stimulation with 10 -6 M isoproterenol (ISOP). Results: The results were compared with normotensive Wistar controls rats (C group, n=10). In basal condition, resting tension, and contraction time (TPT) were greater, while relaxation time (RT 50) tended to be longer in RHT than C group. PRC and ISOP promoted a similar change in muscle function response intensity (Δ) in both groups. ECa 2+ shift did not change TPT in the C group and decreased TPT in the RHT animals; Δ was different between these groups. RT 50 increased in C and decreased in RHT, both without statistical significance; however, Δ was different. Conclusions: These results suggest that hypertrophied myocardial dysfunction may be attibuted to changes in intracellular calcium cycling. © Med Sci Monit, 2010.
dc.languageeng
dc.relationCase Reports and Clinical Practice Review
dc.relation0,619
dc.rightsAcesso aberto
dc.sourceScopus
dc.subjectCalcium isoproterenol
dc.subjectMyocardium function
dc.subjectPapillary muscle
dc.subjectRenovascular hypertension
dc.subjectcalcium ion
dc.subjectchloride
dc.subjectisoprenaline
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectbeta adrenergic stimulation
dc.subjectcalcium cell level
dc.subjectconcentration (parameters)
dc.subjectcontrolled study
dc.subjectextracellular calcium
dc.subjectheart contraction
dc.subjectheart function
dc.subjectheart muscle fiber membrane steady potential
dc.subjectheart muscle relaxation
dc.subjectheart papillary muscle
dc.subjectheart performance
dc.subjectheart ventricle hypertrophy
dc.subjectinotropism
dc.subjectmale
dc.subjectmuscle isometric contraction
dc.subjectnonhuman
dc.subjectrat
dc.subjectrenovascular hypertension
dc.subjectWistar rat
dc.titleHypertrophied myocardium is more dependent on extracellular calcium than the normal cardiac muscle
dc.typeArtigo


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