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目的和方法：通过测定心肌细胞脂质过氧化水平及细胞内钙离子浓度，探讨了阿霉素中毒心肌细胞损伤机制与脂质过氧化及钙离子超负荷的关系。结果：中毒心肌细胞培养基中ＬＤＨ释放量由２５０．２增加到８５３．７μｍｏｌ／Ｌ，ＳＯＤ活力由２５７．５５（Ｕ／ｍｇ·ｐｒｏ）下降到１８５．８８（Ｕ／ｍｇ·ｐｒｏ），丙二醛（ＭＤＡ）含量由１．４０９（ｎｍｏｌ／ｍｇ·ｐｒｏ）增加到１．６３８（ｎｍｏｌ／ｍｇ·ｐｒｏ），细胞内游离钙浓度由２４０．１８（ｎｍｏｌ／Ｌ）增加到１４６０．４０（ｎｍｏｌ／Ｌ）；阿霉素中毒早期仅有〔Ｃａ２＋〕ｉ升高；中毒４ｈ后出现脂质过氧化、心肌损伤加重及〔Ｃａ２＋〕ｉ的进一步升高；结论：心肌细胞内〔Ｃａ２＋〕ｉ早期增高是心肌损伤的始动环节，脂质过氧化与其诱导的〔Ｃａ２＋〕ｉ进一步超负荷之间的恶性循环是心肌损伤加重的根本原因
PURPOSE AND METHODS: The cardiomyocyte lipid peroxidation and intracellular calcium concentration were measured to explore the relationship between the mechanism of doxorubicin-induced cardiomyocyte injury and lipid peroxidation and calcium overload. Results: The release of LDH in the culture medium of cardiomyocytes was increased from 250.2 to 853.7μmol / L, and the SOD activity decreased from 257.55 (U / mg · pro) to 185.88 (U / mg · pro) The content of MDA increased from 1.409 (nmol / mg · pro) to 1.638 (nmol / mg · pro) and the intracellular free calcium concentration increased from 240.18 (nmol / L) to 1460.40 nmol / L). Only the early [Ca2 +] i increased at the early adriamycin poisoning. Lipid peroxidation, myocardial injury and further increase of [Ca2 +] i occurred after 4 hours of poisoning. Conclusion: The intracellular [Ca2 +] i Early increase is the first step in myocardial injury, and the vicious cycle between lipid peroxidation and its further overload with [Ca2 +] i is the root cause of increased myocardial injury