THE ROLE of OXIDATIVE STRESS and LIPID PEROXIDATION IN VENTRICULAR REMODELING INDUCED BY TOBACCO SMOKE EXPOSURE AFTER MYOCARDIAL INFARCTION

dc.contributorUniversidade Estadual Paulista (UNESP)
dc.creatorDuarte, Daniella R.
dc.creatorMinicucci, Marcos Ferreira
dc.creatorGaiolla, Paula Schmidt Azevedo
dc.creatorMatsubara, Beatriz Bojikian
dc.creatorMatsubara, Luiz Shiguero
dc.creatorNovelli, Ethel L.
dc.creatorPaiva, Sergio Alberto Rupp de
dc.creatorZornoff, Leonardo Antonio Mamede
dc.date2014-05-20T13:33:20Z
dc.date2016-10-25T16:51:25Z
dc.date2014-05-20T13:33:20Z
dc.date2016-10-25T16:51:25Z
dc.date2009-01-01
dc.date.accessioned2017-04-05T20:23:35Z
dc.date.available2017-04-05T20:23:35Z
dc.identifierClinics. São Paulo: Hospital Clinicas, Univ São Paulo, v. 64, n. 7, p. 691-697, 2009.
dc.identifier1807-5932
dc.identifierhttp://hdl.handle.net/11449/11406
dc.identifierhttp://acervodigital.unesp.br/handle/11449/11406
dc.identifier10.1590/S1807-59322009000700014
dc.identifierS1807-59322009000700014
dc.identifierWOS:000268725900014
dc.identifierhttp://dx.doi.org/10.1590/S1807-59322009000700014
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/859176
dc.descriptionOBJECTIVE: To evaluate the roles of oxidative stress and lipid peroxidation in the ventricular remodeling that is induced by tobacco smoke exposure after myocardial infarction.METHODS: After induced myocardial infarction, rats were allocated into two groups: C (control, n=25) and ETS (exposed to tobacco smoke, n=24). After 6 months, survivors were submitted to echocardiogram and biochemical analyses.RESULTS: Rats in the ETS group showed higher diastolic (C = 1.52 +/- 0.4 mm(2), ETS = 1.95 +/- 0.4 mm(2); p=0.032) and systolic (C = 1.03 +/- 0.3, ETS = 1.36 +/- 0.4 mm(2)/g; p=0.049) ventricular areas, adjusted for body weight. The fractional area change was smaller in the ETS group (C = 30.3 +/- 10.1 %, ETS = 19.2 +/- 11.1 %; p=0.024) and E/A ratios were higher in ETS animals (C = 2.3 +/- 2.2, ETS = 5.1 +/- 2.5; p=0.037). ETS was also associated with a higher water percentage in the lung (C = 4.8 (4.3-4.8), ETS = 5.5 (5.3-5.6); p=0.013) as well as higher cardiac levels of reduced glutathione (C = 20.7 +/- 7.6 nmol/mg of protein, ETS = 40.7 +/- 12.7 nmol/mg of protein; p=0.037) and oxidized glutathione (C = 0.3 +/- 0.1 nmol/g of protein, ETS = 0.9 +/- 0.3 nmol/g of protein; p=0.008). No differences were observed in lipid hydroperoxide levels (C = 0.4 +/- 0.2 nmol/mg of tissue, ETS = 0.1 +/- 0.1 nmol/mg of tissue; p=0.08).CONCLUSION: In animals exposed to tobacco smoke, oxidative stress is associated with the intensification of ventricular re-remodeling after myocardial infarction.
dc.languageeng
dc.publisherUniversidade de São Paulo (USP), Hospital das Clínicas
dc.relationClinics
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectVentricular function
dc.subjectCoronary occlusion
dc.subjectVentricular dilatation
dc.subjectHypertrophy
dc.subjectHeart failure
dc.titleTHE ROLE of OXIDATIVE STRESS and LIPID PEROXIDATION IN VENTRICULAR REMODELING INDUCED BY TOBACCO SMOKE EXPOSURE AFTER MYOCARDIAL INFARCTION
dc.typeOtro


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