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

Abstract

OBJECTIVE: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 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).CONCLUSION:In animals exposed to tobacco smoke, oxidative stress is associated with the intensification of ventricular remodeling after myocardial infarction.

Tobacco Smoke Induces Ventricular Remodeling Associated with an Increase in NADPH Oxidase Activity

“…Previous studies also suggest that tobacco smoke may induce ventricular remodeling via changes in oxidative stress [18,19]. However, the role that NADPH oxidase plays in cardiac remodeling that is induced by smoking is unknown.…”

“…The potential mechanisms for these alterations include hemodynamic and neurohormonal changes [15], metalloproteinases [16] and mitogen-activated protein kinases activation [17]. These and other effects may be associated with oxidative stress [18,19].…”

“…Animals that have been exposed to tobacco smoke undergo cardiac structural changes that can be observed with electron microscopy; interestingly, these changes can be alleviated with beta-carotene supplementation [18]. Rats exposed to cigarette smoke undergoing experimental myocardial infarction show decreased reduced/oxidized glutathione ratios in heart and liver tissue [19]. However, no studies have addressed whether NADPH oxidase participates in the cardiac remodeling induced by smoking.…”

Aldosterone is not Involved in the Ventricular Remodeling Process Induced by Tobacco Smoke Exposure

“…Interestingly, tobacco smoke did not increase myocardial inflammatory cytokines in our study. Although we have already observed these cytokine patterns in previous studies, ICAM-1 expression has not yet been evaluated in tobacco exposure models [8,11]. Importantly, the expression of adhesion molecules is essential for the influx of inflammatory cells into the myocardium.…”

“…The mechanisms involved in this remodeling process are not completely known. Potential mechanisms for these alterations include inflammation [8,11], oxidative stress [8,11], metalloproteinase [5] and mitogen-activated protein kinase activation [6], and hemodynamic and neurohormonal changes, such as renin-angiotensinaldosterone system (RAAS) activation [12].…”