The effect selenium in the form of sodium selenite on central hemodynamic conditions and coronary artery flow was studied in pig hearts infarcted by a ligature of the ramus interventricularis anterior. Infusions of sodium selenite solutions at levels of 1-3 mg/kg body wt improved the survival of infarcted pigs. Both short-term and long-term protective effects of selenite could be demonstrated. It is of potential therapeutic importance that sodium selenite administration suppresses the electrical vulnerability of the cell membrane, notably the occurrence of ventricular late potentials in the ischemic border zone. Coronary blood circulation, as evidenced by an increase of heart rate and coronary artery dilatation and peripheral vasodilation was also improved. The pulsatile coronary blood flow thus is altered, increasing total perfusion of the infarcted heart. Initial observations with human subjects suggest that selenium deficiency is a factor in the pathogenesis of ischemic and arteriosclerotic heart disease. In 54 hospitalized patients with clinical diagnosis of acute myocardial infarction, serum selenium levels were 670 +/- 266 nmol/L, as compared to 981 +/- 209 nmol/L in 93 healthy controls. In 32 patients with general arteriosclerosis, the serum Se level was 375 +/- 85 nmol/L, in 64 patients with arteriosclerotic occlusional disease in the leg region, 366 +/- 85 nmol/L, respectively. Serum selenium levels of healthy subjects were found to be age- and sex dependent. In men, the selenium concentrations reached maximum levels of 1083 nmol/L in the 41-50 y age group. In women in the same age group, the serum Se level was 1385 nmol/L. Evidence is presented to suggest that selenium is preventing oxidative damage of heart cell membranes by lipid peroxidation.