Chronic cardac adaptation to acute aorta regurgitation in rats

Abstract

Myocardial remodeling following volume overload is not well known. This is a relevant matter in countries where cardiac valve insufficiency is still prevalent. We hypothesized that in vivo left ventricular dysfunction caused by aorta regurgitation (AR) in rats is not associated with pulmonary congestion. Also, it is possible that ventricular dysfunction is associated with changes in intracellular calcium homeostasis without myocardial fibrosis. The aims of the present study are: 1-to evaluate the temporal evolution of ventricular adaptation to acute aorta regurgitation, identifying the markers of decompensated hypertrophy, 3-to identify the myocardial collagenolytic activity early after volume overload; 4-to analyze the pattern of heavy chain myosin and the RNA expression for phospholamban, ryanodine receptors and SERCA2. Methods: after surgical AR or SHAM surgery, Wistar rats will be followed for 16 weeks. Serial Doppler-echocardiograms will be performed. After this period, animals will be killed and myocardial samples will be saved for biochemical and histological analysis. One week after the surgery, six animals from each group will be killed for analysis of myocardial collagenolytic activity. The Intitutional's Ethics Committee for Research on Animals approved all procedures (AU)