The effect of captopril (Cap) on electric activity of cultured rat myocardial cells under anoxia and reoxygenation was studied with standard microelectrode techniques. Results showed that anoxic solution caused lowerings of MDP, APA, and Vmax, and a shortening of APD50. All myocytes revealed multiform arrhythmias, and most cells stopped beating within 30 min, while only 40% of the cells exhibited arrhythmias but none stopped beating in the presence of 40 mg.L-1 under the same condition. During reoxygenation, most cells resumed beating in 10 min but some of these cells stopped beating again. The electric activities in rebeating cells during reoxygenation for 30 min were lower than those in normoxic cells. Cap (40 mg.L-1)-treated cells rebeat quickly after reoxygenation and no cell stopped beating any more, with parameters higher than those in untreated cells. These results demonstrate that Cap yields some beneficial effects on preventing anoxia and reoxygenation injury in cultured rat myocardial cells.