Reduced Force Generating Capacity in Myocytes From Chronically Ischemic, Hibernating Myocardium

The contractile dysfunction of the hibernating myocardium in situ results from local environmental factors, but also from intrinsic cellular remodelling that may determine reversibility. Previous studies have suggested defects in myofilament Ca responsiveness. We prepared single myocytes from control (CTRL, npigs=7) and from hibernating myocardium (HIB, npigs=8), removed the membranes and measured isometric force development during direct activation of the myofilaments. One- and 2-dimensional polyacrylamide gel electrophoresis and specific phosphoprotein immunoblotting were performed on tissue homogenates from matched samples. Cellular ultrastructure was evaluated using electron microscopy. Normalized for cross-sectional area, passive force was not different but maximal isometric force was significantly reduced in myocytes from HIB (11.6±1.5 kN/m versus 18.7±1.6 kN/m in CTRL, P