Early and excessive catecholamine stimulation of the heart increases the overcharge blood pressure and volume on ventricles. Thus worsening myocardial ischemia by causing the death of myocytes. With connective tissue deposition and progressive reduction of heart output. Carvedilol, a b and alpha1-blocker non heart-selective, has been associated to improvement on myocardial function on left ventricle hypertrophy regression. The aim of this study was to evaluate the action of carvedilol in rats undergone to an experimental model of hypertrophic cardiomyopathy by pressure overcharge, through subdiaphragmatic aortic coarctation. Wistar rats (65 animals) divided into four groups: non- coarcted/ treated with placebo, coarcted / treated with placebo, coarcted / treated with 0.1mg kg-1 of carvedilol and coarcted / treated with 1mg/kg of carvedilol. After surgery and 20 days of treatment, the animals were euthanized and samples were collected, fixed in formol 10% and processed using picrossirius staining to quantify connective tissue on left and right ventricles. On those coarcted animals / treated with placebo, there was a rise on the percentage of connective tissue on left and right ventricles; on coarcted animals / treated with 0.1mg kg-1 of carvedilol there was a partial reduction on the amount of collagen tissue of left and right ventricles; and on those coarcted animals / treated with 1mg kg-1 of carvedilol there was a significant reduction on the amount of collagen tissue of left ventricle.
carvedilol; myocardial hypertrophy; rats; coarctation
