Abstract
Objective: Myocardial ischemia is an acute condition that, if not treated in a timely manner, produces the loss of heart tissue which can lead to heart failure or death of the patients. Our group has studied fibrates, exogenous ligands of PPAR, as an alternative to reduce processes associated with inflammation and we interested to know the exogenous ligand effect over damage in the cardiac tissue by RAS system. To study the effect of PPAR alpha ligand; clofibrate, on renin angiotensin system and on the structural morphology of the heart in myocardial infarcted subjects. Design and method: Male Wistar rats were separated in two groups: 1.- Sham, 2.- Myocardial infarct by coronary artery ligation. Seven days after, the rats were subdivided in vehicle (Vh)- or clofibrate treatment (Clof 100 mg/kg/day) administered for seven more days. At the end of the treatment (14 days in total), serum and left ventricle were analyzed. Results: Angiotensin converting enzyme (ACE), AT1 receptor and Ang II decreased in MI-Clof vs. MI-Vh, whereas non-classic RAS system components: ACE2, AT2 receptor, bradykinin, and Ang-(1–7) augmented in MI-Clof with respect to MI-Vh. VEGF also raised in clofibrate-treated animals. Clofibrate treatment preserved the structure of the sarcomere (fiber). Conclusions: Clofibrate treatment to MI rats exerts an antifibrotic effect and augmented the expression of non-classical axis of RAS system.
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