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The Role of Oxidative Stress and Lipid Peroxidation in Ventricular Remodeling Induced by Tobacco Smoke Exposure after Myocardial Infarction

2009; Elsevier BV; Volume: 64; Issue: 7 Linguagem: Inglês

10.1590/s1807-59322009000700014

1980-5322

Daniella R. Duarte, Marcos Ferreira Minicucci, Paula S. Azevedo, Beatriz B. Matsubara, Luiz Shiguero Matsubara, Ethel Lourenzi Barbosa Novelli, Sérgio Alberto Rupp de Paiva, Leonardo A. M. Zornoff,

Cardiac Ischemia and Reperfusion

To evaluate the roles of oxidative stress and lipid peroxidation in the ventricular remodeling that is induced by tobacco smoke exposure after myocardial infarction. 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. Rats in the ETS group showed higher diastolic (C = 1.52 ± 0.4 mm2, ETS = 1.95 ± 0.4 mm2; p=0.032) and systolic (C = 1.03 ± 0.3, ETS = 1.36 ± 0.4 mm2/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). In animals exposed to tobacco smoke, oxidative stress is associated with the intensification of ventricular remodeling after myocardial infarction.