Rui T, Yang Y Z, Zhou T S, Yang X Y, Chen H Z
Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Shanghai Medical University, China.
Zhongguo Yao Li Xue Bao. 1994 Jul;15(4):375-8.
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.
采用标准微电极技术研究了卡托普利（Cap）对缺氧复氧条件下培养的大鼠心肌细胞电活动的影响。结果显示，缺氧溶液导致最大舒张电位（MDP）、动作电位幅度（APA）和最大上升速率（Vmax）降低，50%动作电位时程（APD50）缩短。所有心肌细胞均出现多种形式的心律失常，大多数细胞在30分钟内停止跳动，而在相同条件下，存在40mg·L-1卡托普利时，只有40%的细胞出现心律失常，但无一停止跳动。复氧过程中，大多数细胞在10分钟内恢复跳动，但其中一些细胞再次停止跳动。复氧30分钟时再次跳动的细胞的电活动低于常氧细胞。用40mg·L-1卡托普利处理的细胞复氧后迅速再次跳动，且无细胞再次停止跳动，其各项参数高于未处理细胞。这些结果表明，卡托普利对预防培养的大鼠心肌细胞缺氧复氧损伤具有一些有益作用。
