Pathogenesis and prophylaxis of cardiac lesions in stress

Emotional or painful stress excites the brain centers which trigger stress reactions, this excitement being followed by an increase in catecholamine concentration. The following chain of events is thought to occur under the influence of the catecholamine excess: activation of lipid peroxidation in the membranes; labilization of lysosomes; damage to sarcolemmal membranes which are responsible for calcium transport; increased calcium concentration in the heart sarcoplasm. The contraction of myofibrils, the decrease in efficiency of ATP resynthesis in the mitochondria, and the activation of phosphorylase and proteases all arise from the calcium excess. This results in necrotic foci and alterations of heart function. The damages can be effectively prevented by suppression of stress-responding centers with gamma-aminobutyric acid, blockade of beta receptors with propranolol, inhibition of lipid peroxidation by antioxidants, inhibition of proteolytic lysosomal enzymes with trasilol, or blocking of calcium entry into the myocytes with verapamil. The possible application to clinical practice of chemical prophylaxis of stress damage in the heart is discussed.