Abstract 861: Inner Mitochondrial Collapsing in Response to Acute Overstretch of Rat Ventricular Papillary Muscles

Abstract

Introduction: The effect of acute ventricular volume overload on organelles such as myofibrils and mitochondria are incompletely understood. Purpose: We performed acute overstretch on cardiac papillary muscle to investigate the functional and morphological changes. Methods: We used male SD-rats (10-12 weeks old) and dissected papillary muscles from the right ventricle. A papillary muscle preparation was stretched to Lmax. We overstretched it within 2 seconds up to 110% of Lmax (110%Overstretch; 110%OS) or 120% of Lmax (120%OS), and stimulated it (1Hz, 36°C) with tension measurement, compared with Lmax group. After the measurement of tension, we analyzed the morphological changes in muscle fibers and organelles using a Transmission electron microscopy (TEM). Results: The active tension after overstretch was immediately decreased to 67.8±3.8% in 110%OS, and to 17.3±4.0% in 120%OS. In TEM study, muscle fibers kept their well-organized structures and the sarcomere length was stretched to 2.4 μm in 110%OS, and to 2.6 μm in 120%OS. In contrast, in 110%OS, inner mitochondrial density was lower than that in Lmax, indicating swelled mitochondria. In 120%OS, inner mitochondrial empty space with vacuolation was found in the large area of myocardium, indicating that inner mitochondria cristae were susceptible to mechanical stress-induced deterioration. Conclusions: Acute overstretch of rat papillary muscles causes inner mitochondrial collapsing with preserved the sarcomere structure. It could account for the mechanisms of acute volume-overloaded heart failure.