Exposure time and ventricular remodeling induced by tobacco smoke exposure in rats
Nenhuma Miniatura disponível
Data
2008-03-01
Autores
Castardeli, Edson [UNESP]
Duarte, Daniella R. [UNESP]
Minicucci, Marcos Ferreira [UNESP]
Gaiolla, Paula Schmidt Azevedo [UNESP]
Matsubara, Beatriz Bojikian [UNESP]
Matsubara, Luiz Shiguero [UNESP]
Campana, Alvaro O. [UNESP]
Paiva, Sergio Alberto Rupp de [UNESP]
Zornoff, Leonardo Antonio Mamede [UNESP]
Título da Revista
ISSN da Revista
Título de Volume
Editor
Int Scientific Literature, Inc
Resumo
Background: We investigated the effects of length of exposure to tobacco smoke on the cardiac remodeling process induced by exposure to cigarette smoke in rats.Material/Methods: Rats were separated into 4 groups: nonsmoking (NS) 2 (n=25; control animals not exposed to tobacco smoke for 2 months), smoking (S)2 (n=22; rats exposed to smoke from 40 cigarettes/d for 2 months), NS6 (n=18; control animals not exposed to tobacco smoke for 6 months), and S6 (n=25; rats exposed to smoke from 40 cigarettes/d for 6 months). All animals underwent echocardiographic, isolated heart, and morphometric studies. Data were analyzed with a 2-way analysis of variance.Results: No interaction among the variables was found; this suggests that length of exposure to tobacco smoke did not influence the effects of exposure to smoke. Values for left ventricular diastolic diameter/body weight and left atrium/body weight were higher (p=0.023 and p=0.001, respectively) in smoking (S2 and S6) than in nonsmoking animals (NS2 and NS6). Left ventricular mass index was higher (p=0.048) in smoking than in nonsmoking animals. In the isovolumetrically beating ventricle, peak systolic pressure was higher (p=0.034) in smoking than in nonsmoking animals. Significantly higher values were found for left ventricular weight (p=0.017) and right ventricular weight (p=0.001) adjusted for body weight in smoking as opposed to nonsmoking animals. Systolic pressure was higher (p=0.001) in smoking (128 +/- 14 mm Hg) than in nonsmoking animals (112 +/- 11 mm Hg).Conclusions: Length of exposure to cigarette smoke did not influence cardiac remodeling caused by exposure to sm oke in rats.
Descrição
Palavras-chave
ventricular function, fibrosis, ventricular dilatation
Como citar
Medical Science Monitor. Albertson: Int Scientific Literature, Inc, v. 14, n. 3, p. BR62-BR66, 2008.