Myocardial Failure and Excitation-Contraction Uncoupling During the Course of Canine Endotoxin and Hemorrhagic Shock

Abstract

Failure of the myocardium and vascular smooth muscle to maintain and regulate intracellular calcium homeostasis (intracellular calcium overload) results in cell death and tissue necrosis. Conditions under which this phenomenon occurs in cardiac muscle have been documented in such diverse etiologies as catecholamine necrosis of the myocardium, prolonged periods of hypoxia, low flow states and after reperfusion of a previously ischemic vascular bed (1). Such conditions exist during the course of both hemorrhagic and endotoxin shock. The later stages of septic and endotoxin shock are associated with increasing peripheral vascular resistance and decreasing cardiac output (2). Experimental and clinical hemorrhagic shock are both associated with prolonged periods of low flow and then with subsequent transfusion, reperfusion of a previously ischemic vascular bed occurs (3). Thus in both of these shock syndromes, the potential for intracellular calcium overload exists.