Contractility changes of the right and left ventricular muscle after chronic myocardial infarction

ABSTRACT

Contractility changes and adaptive responses resulting from acute left ventricular (LV) myocardial infarction are not restricted to the LV myocardium. 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 investigated the mechanical activity of RV and LV isolated papillary muscles from 30-day infarcted male Wistar, 3-4-months old rat hearts. LV myocardial infarction was produced by ligature of the descending anterior branches of the left coronary artery (INF group). Control animals were submitted to sham surgery (SO group). Both groups were studied 30 days after the infarction procedure. Post-infarction hypertrophy was evaluated by measuring the cell diameters in the nuclear region. Contractility changes were analyzed by determining the isometric force (F) and the rate of force development (dF/dt) of papillary muscles from LV and 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 contractures obtained during caffeine perfusion (2.5 mM) and were used to assess changes at the contractile protein level. The activity of the sarcoplasmic reticulum was evaluated by using the post-rest potentiation phenomenon. Hypertrophy occurred in both ventricles after infarction, with the RV chamber showing a pressure overload pattern while LV myocytes developed a volume overload pattern. F and dF/dt of LV papillary muscles decreased after infarction but did not change in the RV preparations. Positive inotropic changes obtained with increasing Ca2+ concentrations and the development of tetanic tension were reduced after infarction only in LV papillary muscles. The relative potentiation of post-rest contractions was only affected in the LV myocardium showing a decrease after infarction. These results suggest that different adaptive changes occur in the LV and RV myocardium after infarction. While the RV myocardium maintains its contractility the LV myocardium displays a depressed mechanical activity problably due to changes at the contractile mechinery level and to alterations in the Ca2+ handling process.