In the initial phase of its action on the contracting myocardium the inductor of lipid peroxidation (LPO) H2O2 displays marked positive ino- and chronotropic as well as relaxant effects which are, therefore, close to catecholamine effects. Since catecholamines activate LPO it suggests that such activation may be involved in the mechanism of their physiologic action. The prolongation of H2O2 action inevitably leads to the development of bradycardia and bradyarrhythmic arrhythmia which may ultimately end in cardiac arrest. The atrial resistance to H2O2 in animals exposed to stress is considerably diminished: in response to this inductor of LPO such animals develop more pronounced bradyarrythmic arrhythmia and cardiac arrest without the stage of the initially positive inotropic effect. The preincubation of the contracting atrium by HP-6, a LPO inhibitor of the hydroxypyridine class, checks the development of bradyarrhythmic arrhythmia and in many cases prevents cardiac arrest. Taken as a whole these data suggest that LPO activation may play an important role in the pathogenesis of cardiac rhythm disorders which may serve as substantiation for the use of antioxidants in the treatment and prevention of arrhythmias.