Over a 10-week period, female Wistar rats received a diet containing a low level of selenium, cofactor of the antioxidant enzyme glutathione peroxidase (GPx) in order to examine the influence of deficiency of this trace element (i) on tissue antioxidant enzyme defence systems, and (ii) on the susceptibility of the myocardium to ischemia-reperfusion injury. At the end of the dietary treatment, hearts were perfused at constant flow (11 ml/min) before being subjected to 15 min of global normothermic ischemia, followed by 30 min of reperfusion. The effects of selenium deficiency were estimated by studying functional recovery of various cardiac parameters (left ventricular developed pressure LVDevP, heart rate HR, and the product HR x LVDevP), as well as ultrastructural tissue characteristics. Furthermore, superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities were measured at the end of the reperfusion period. Results suggest that: (a) the activity of GPx is decreased by selenium deficiency while SOD activity remains unchanged, (b) the recovery of cardiac function and myocardial ventricular ultrastructure during reperfusion are altered in the selenium-deficient group compared to controls. These results illustrate the crucial role that selenium, the co-factor of one of the major antioxidant enzymes of the myocardium, plays in determining the vulnerability of the heart to ischemia and reperfusion.