摘要
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。
100μmol/L adriamycin(ADR)resulted in a decrease of cardiac functions and in- crease of lipid peroxide(MDA)content with no change of total calcium in isolated perfused myocardi- um,indicating the early mechanisms of ADR toxicities are related to free radicals rather than Ca^(2+) overload induced by excessive Ca^(2+) influx.We also showed no obvious damage of sarcolemma in ADR perfused myocardium,suggesting the early inside injury of myocardial cells.ADR induced rapid and transient increase of cardiac contraction force and this phenomenon is consistent with ADR-induced Ca^(2+) release from cardiac sarcoplasmic reticulum.
关键词
阿霉素
心肌病
自由基损伤
adriamycin
cardiomopathy
Ca^(2+) overload
free radical injury
Ca^(2+) release from sarcoplasmic reticulum
