The World Health Organization estimates that one-third of the world population are smokers and that smoking is the leading cause of preventable death in the world. It is known that smoking increases the risk of death from cardiovascular disease, but little is known about the effects of cigarette smoke directly into the myocardium .In a normal heart, 60-90% of the ATP come from the oxidation of fatty acids (FA). In pathological conditions, there is a reduction in the oxidation of fatty acids and an increase in glucose utilization. This occurs in the early stages of cardiac remodeling as a way to protect the heart. In later stages, the FA were not oxidized, accumulate form of triglycerides, leading to lipotoxicity. Moreover, at this moment, glucose metabolism may be compromised, damaging myocardial function. It is possible that exposure to cigarette smoke induces alterations in energy metabolism, specially through abnormalities in fatty acids and glucose metabolism, since it plays an important role in cardiac remodeling. The objectives are: 1) to evaluate cardiac remodeling through morphological and functional echocardiographic variables and histological variables, 2) evaluate the process of glucose utilization by variables such as Akt-1, AMPK, GLUT4, eNOS , fosfofrutokinase and pyruvate dehydrogenase. Twenty Wistar rats will be allocated into 2 groups: group of animals exposed to cigarette smoke (CS), and group unexposed animals will smoke cigarettes (C). After 2 months the animals are subjected to: a) echocardiographic b) Blood pressure flow c) histological study using immunofluorescence d) Western Blot for Akt-1, AMPK, GLUT4, eNOS, e). spectrophotometry for fosfofrutokinase, pyruvate dehydrogenase and ATP synthases activities.
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