不同累积量的阿霉素所致心肌细胞超微结构和电生理改变

选用Wistar雄性大鼠49只,随机分为对照组17只,每周阿霉素2mg/kg;用药3周者13只(ADR3组);6周者10只(ADR6组);10周者9只(ADR10组),末次注射后间隔一周处死动物并取材。大体解剖表明对照组及ADR3组正常;ADR0组3只有腹水;ADR10组7只有心包积液、胸水、腹水,提示心力衰竭。超微结构显示对照组及ADR3组基本正常;APD6及ADR10有明显异常,细胞内水肿,染色质块状凝集,肌丝排列紊乱、溶解、断裂,线粒体肿胀、嵴断裂、空泡变、膜破裂等。电生理、快反应动作电位是ADR6和ADR10两组的ADR50明显延长(P<0.05),慢反应动作电位ADR6和ADR10两组的APD50、APD90明显延长,Vmax明显增加(P<0.05),其他电生理参数无明显改变。结果提示心肌细胞电生理和超微结构的变化与药物累积剂量相关。毒性反应与增加心肌细胞钙内流有关。

PROTECTIVE EFFECT OF SHENG MAI SAN ON ADRIAMYCIN-INDUCED CARDIOTOXICITY——AN EXPERIMENTAL STUDY

By measuring the contents of lipid-bound sialic acid (LSA), malonyldialdehyde (MDA), activities of glutathione peroxidase (GSH-px) and superoxide dismutase (SOD) of the myocardial cells, it has been shown that Sheng Mai San can protect the myocardial cells from the adriamycin-induced cardiotoxicity ultrastructrally, inhibit their metabolism of lipid-bound sialic acid and improve the scavenging ability of myocardial cells for semiquinoid free radicals.