Stress-induced injury of pig myocardium is accompanied by increased lipid peroxidation and depletion of mitochondrial ATP.

The aim of the study was to investigate the mechanisms of myocardial lesions induced by stress in conscious, intact pigs. The animals were subjected to 24 h immobilization, controls were kept in normal conditions. The pigs were killed by electric shock and exsanguination. Lipid peroxidation products: malondialdehyde (MDA), conjugated dienes (CDB), fluorescent end products (RF) and adenine nucleotides (ATP, ADP) were measured in the left ventricular myocardium which was also subjected to histoenzymatic and electron microscopic examination. In stressed animals as opposed to the control group, alterations in ultrastructure and diminution of mitochondrial ATP have been found, together with augmented formation of MDA and CDB reflecting increased free radical generation. These changes may be the component of stress-induced myocardial injury.