CONTRACTILITY CHANGES OF THE RIGHT AND LEFT-VENTRICULAR MUSCLE AFTER CHRONIC MYOCARDIAL-INFARCTION

Contractility changes and adaptive responses resulting from acute left ventricular (LV) myocardial infarction are not restricted to the LV m yocardium. The reduced LV function increases the right ventricular (RV ) pressure load and neurohumoral factors, activated by the infarction episode, might have pan-cardiac effects. In the present study we inves tigated the mechanical activity of RV and LV isolated papillary muscle s from 30-day infarcted male Wistar, 3-4-months old rat hearts. LV myo cardial infarction was produced by ligature of the descending anterior branches of the left coronary artery (INF group). Control animals wer e submitted to sham surgery (SO group). Both groups were studied 30 da ys after the infarction procedure. Post-infarction hypertrophy was eva luated by measuring the cell diameters in the nuclear region, Contract ility changes were analyzed by determining the isometric force (F) and the rate of force development (dF/dt) of papillary muscles from LV an d RV. The effects of variations in extracellular Ca2+. concentrations (0.6, 1.25, 2.5 and 3.75 mM) were determined on twitches and tetanic c ontractures obtained during caffeine perfusion (2.5 mM) and were used to assess changes at the contractile protein level. The activity of th e sarcoplasmic reticulum was evaluated by using the post-rest potentia tion phenomenon. Hypertrophy occurred in both ventricles after infarct ion, with the RV chamber showing a pressure overload pattern while LV myocytes developed a volume overload pattern. F and dF/dt of LV papill ary muscles decreased after infarction but did not change in the RV pr eparations. Positive inotropic changes obtained with increasing Ca2+ c oncentrations and the development of tetanic tension were reduced afte r infarction only in LV papillary muscles. The relative potentiation o f post-rest contractions was only affected in the LV myocardium showin g a decrease after infarction. These results suggest that different ad aptive changes occur in the LV and RV myocardium after infarction. Whi le the RV myocardium maintains its contractility the LV myocardium dis plays a depressed mechanical activity probably due to changes at the c ontractile machinery level and to alterations in the Ca2+ handling pro cess.