Right ventricular contractile protein function in rats with left ventricular myocardial infarction.

We studied contractile function in cardiac trabeculae isolated from the right ventricles (RV) of rats with experimental heart failure (HF) induced by left ventricular (LV) myocardial infarction (24 wk post-MI; n = 6) and from sham-operated rats (n = 7). Sarcomere length (SL) was measured by laser diffraction techniques, and force (F) was measured by silicon strain gauge. SL was kept constant at all times by computer feedback control. HF was associated with marked LV dilation and pulmonary congestion. In intact, RV twitching trabeculae, HF was associated with a depression of the F-SL relation at extracellular Ca2+ concentration ([Ca2+]o) = 1.5 mM and a depression of the F-[Ca2+]o relation at SL = 2.0 microns. HF was also associated with a significant depression of the F-intracellular [Ca2+] relation at SL = 2.0 microns measured after chemical permeabilization of these RV trabeculae (skinned fibers). Our results suggest that reduced force development in this model of HF is due, in part, to depressed function of the contractile filaments.