The effect of myocardial infarction sustained by rats on the resistance of their isolated auricles to H2O2, an inductor of lipid peroxidation (LP), was studied. Atrial resistance to the LP inductor depends on the level of developed tension (DT) and the decrease of DT leads to augmentation of atrial resistance to the arrhythmogenic effect of LP. The experimental myocardial infarction causes appreciable disturbances in the function of automatism of the auricles, 60% of which lose their capability of spontaneous contractile activity. When compared with the control under equal DT, the auricles of the "infarction" series are less resistant to H2O2: the time of arrhythmias and arrests in them are 2.3 times as much as in the control. In infarction, the pretreatment with ionol reduces both the quantity of the auricles which stopped before H2O2 administration and the quantity of the auricles responding by arrhythmia to LP induction. The data point to the possibility of the use of antioxidants for preventing arrhythmias in experimental myocardial infarction.