Calcium Flux Across the Myocardial Cellular Membrane During Cardioplegic Cardiac Arrest

Because of its role as a mediator of information between the cellular membrane and the sarcoplasm during the action potential, which leads to muscle contraction, and in its capacity as a regulating factor for the actin-myosin interaction [3], calcium (Ca) occupies a central position in the electrophysiology of myocardial contraction — especially in the electromechanical coupling. Ca is predominantly an extracellular cation partly bound to the myocardial cellular membrane (Ca pools). Following an action potential, an inward Ca current corresponding in time with the plateau of the action potential occurs. The influx of Ca ions across the membrane into the sarcoplasm proceeds via the so-called slow Ca channels. The Ca ions effect a progressive release of “free” sarcoplasmic Ca+ + ions from the intracellular depots (sarcoplasmic reticulum and the mitochondria), and an increased binding of Ca ions to troponin C — a decisive step in the electromechanical coupling. During muscle relaxation, Ca ions are withdrawn from the sarcoplasm into the intracellular depots and out of the cell. These physiological Ca shifts in the living cell maintain a normal intracellular Ca concentration of about 0.1–1 μmol [6]. Ischemia causes myocardial injuries which may result in pathological Ca shifts with a tendency towards a high intracellular Ca accumulation during reperfusion [4, 5, 8, 9], the extent of Ca accumulation being dependent on the severity of the ischemic injury sustained. The goal of myocardial protection is the preservation of myocardial ultrastructure and function. The restoration of the intracellular ions following reperfusion to the control values is a sine qua non of normal cellular function.