The ability of amiodarone to prevent pathological changes and oxidative stress after isoproterenol (ISO)-induced myocardial injury was investigated in rats. A better understanding of the processes involved in the pathophysiology of myocardial infarction has led to the search for drugs that can limit the extent of myocardial injury. Amiodarone was administered to groups of rats groups once per day for 30 days. On days 29 and 30, the rats of the ISO control and drug treatment groups were administered 180 mg/kg ISO subcutaneously at an interval of 24 h for two consecutive days. In the control groups, clinical indicators, such as creatine kinase-isoenzymes and troponin-I, were found to be statistically higher than in the drug groups. Parallel to this increase in indicators, a significant decrease in glutathione levels and activities of superoxide dismutase and an increase in malondialdehyde level were detected. Biochemical and histopathologic results in the ISO-induced model of myocardial injury emphasize the beneficial action of amiodarone as a cardioprotective agent.