Cellular and Molecular Mechanisms of High Pressure Inotropy in Cardiac Muscle

Cardiac muscle subjected to increased hydrostatic pressure from 2 to 150 atmospheres respond with an increase in developed tension, a phenomenon we refer to as high pressure inotropy or HPI. Experiments were performed on papillary muscles isolated from adolescent rabbit hearts to test the possibility that HPI is due to a preferential action of pressure to partially inhibit the activity of the sodium-potassium pump of the cell membrane leading to calcium accumulation through reduced sodium-calcium exchange. Ouabain, a cardiac glycoside known to inhibit pump activity, prevented the development of HPI when applied before pressure was increased. Both ouabain and pressure altered the time course of mechanical restitution and the development of the resting state contraction in a similar manner that could be mimicked by a computer model when the calcium extrusion ordinarily occurring during each cardiac cycle was substantially retarded. Finally, we reported on progress made to develop a microfluorimeter for measuring cytosolic calcium in single cardiac myocytes under hyperbaric conditions. Keywords: Membranes biology.