阿霉素(100μM)可使离件心脏功能降低,心肌脂质过氧化物(MDA)含量明显增高,但钙含量未见增加,提示阿霉素早期心肌损伤的机制可能首先与自由基有关而不是胞外Ca~(2+)大量内流引起的Ca~(2+)超负荷。本实验还显示心肌细胞膜无明显破坏,推测阿霉素的早期作用部位主要在细胞内。给药后心肌收缩力迅速地、一过性地增高,与作者等以前观察到的阿霉素引起肌浆网Ca~(2+)释放特点相似。本文讨论了肌浆网Ca~(2+)释放与阿霉素心肌病的关系。 Doxorubicin (100μM) decreased heart function and increased myocardial lipid peroxidation (MDA), but no increase in calcium content, suggesting that the mechanism of early myocardial damage in adriamycin may be related to free radical It is not Ca 2+ overload caused by extracellular Ca 2+ influx. The experiment also showed no obvious damage to the myocardial cell membrane, presumed that adriamycin early site of action mainly in the cell. Myocardial contractile force rapidly and transiently increases after administration, which is similar to the previous observation that doxorubicin causes the release of Ca 2+ in sarcoplasmic reticulum. This article discusses the relationship between Ca2 + release from sarcoplasmic reticulum and adriamycin cardiomyopathy.