Rafacho Bruna P M, Azevedo Paula S, Polegato Bertha F, Fernandes Ana A H, Bertoline Maria A, Fernandes Denise C, Chiuso-Minicucci Fernanda, Roscani Meliza G, Dos Santos Priscila P, Matsubara Luiz S, Matsubara Beatriz B, Laurindo Francisco R M, Paiva Sergio A R, Zornoff Leonardo A M, Minicucci Marcos F
Internal Medicine Department, Botucatu Medical School, Univ Estadual Paulista, Botucatu, Brazil.
Cell Physiol Biochem. 2011;27(3-4):305-12. doi: 10.1159/000327957. Epub 2011 Apr 1.
Recent studies have assessed the direct effects of smoking on cardiac remodeling and function. However, the mechanisms of these alterations remain unknown. The aim of this study was to investigate de role of cardiac NADPH oxidase and antioxidant enzyme system on ventricular remodeling induced by tobacco smoke.
Male Wistar rats that weighed 200-230 g were divided into a control group (C) and an experimental group that was exposed to tobacco smoke for a period of two months (ETS). After the two-month exposure period, morphological, biochemical and functional analyses were performed.
The myocyte cross-sectional area and left ventricle end-diastolic dimension was increased 16.2% and 33.7%, respectively, in the ETS group. The interstitial collagen volume fraction was also higher in ETS group compared to the controls. In addition to these morphological changes, the ejection fraction and fractional shortening were decreased in the ETS group. Importantly, these alterations were related to augmented heart oxidative stress, which was characterized by an increase in NADPH oxidase activity, increased levels of lipid hydroperoxide and depletion of antioxidant enzymes (e.g., catalase, superoxide dismutase and glutathione peroxidase). In addition, cardiac levels of IFN-γ, TNF-α and IL-10 were not different between the groups.
Cardiac alterations that are induced by smoking are associated with increased NADPH oxidase activity, suggesting that this pathway plays a role in the ventricular remodeling induced by exposure to tobacco smoke.
近期研究评估了吸烟对心脏重塑和功能的直接影响。然而，这些改变的机制仍不清楚。本研究的目的是探讨心脏NADPH氧化酶和抗氧化酶系统在烟草烟雾诱导的心室重塑中的作用。
将体重200 - 230克的雄性Wistar大鼠分为对照组（C）和暴露于烟草烟雾两个月的实验组（ETS）。在两个月的暴露期后，进行形态学、生化和功能分析。
ETS组心肌细胞横截面积和左心室舒张末期内径分别增加了16.2%和33.7%。ETS组的间质胶原容积分数也高于对照组。除了这些形态学变化外，ETS组的射血分数和缩短分数降低。重要的是，这些改变与心脏氧化应激增加有关，其特征是NADPH氧化酶活性增加、脂质过氧化氢水平升高和抗氧化酶（如过氧化氢酶、超氧化物歧化酶和谷胱甘肽过氧化物酶）耗竭。此外，两组之间心脏IFN-γ、TNF-α和IL-10水平无差异。
吸烟诱导的心脏改变与NADPH氧化酶活性增加有关，表明该途径在暴露于烟草烟雾诱导的心室重塑中起作用。
