Lambertenghi-Deliliers G, Zanon P L, Pozzoli E F, Bellini O, Praga C
Tumori. 1978 Feb 28;64(1):15-24. doi: 10.1177/030089167806400102.
The clinical use of adriamycin (AM) is limited by a possible dose-dependent myocardiopathy. Severe lesions of ventricular myocardium widely described by electron microscopy have been correlated to irreversible congestive heart failure. On the other hand, the atrial contractile elements which differ from the ventricular ones because of the presence of the so-called specific granules have rarely been considered. In the work described in this paper, adriamycin was injected into rabbits and mice according to schedules of chronic toxicity. At the end of the treatment the atrial myocells presented diffuse ultrastructural lesions of mitochondria, sarcoplasmic reticulum and myofibrillar bundles. These alterations might be caused by the ribonucleoprotein synthesis inhibition, by a direct drug toxicity or by an energetic crisis due to early mitochondrial lesions. Besides, adriamycin produces a decrease of the specific atrial granules that play a hypothetic role in the metabolism of myocardial cells. However, lack of information about the contents and the exact function of atrial granules does not allow us to conclude that their decrease in treated animals has a pathogenetic significance in myocardiopathy induced by adriamycin.
阿霉素（AM）的临床应用受到可能的剂量依赖性心肌病的限制。电子显微镜广泛描述的心室心肌严重病变与不可逆的充血性心力衰竭相关。另一方面，由于存在所谓的特异性颗粒而与心室收缩成分不同的心房收缩成分很少被考虑。在本文所述的研究中，按照慢性毒性方案给兔子和小鼠注射阿霉素。治疗结束时，心房肌细胞出现线粒体、肌浆网和肌原纤维束的弥漫性超微结构病变。这些改变可能是由于核糖核蛋白合成抑制、直接药物毒性或早期线粒体病变导致的能量危机引起的。此外，阿霉素会使在心肌细胞代谢中起假设作用的特异性心房颗粒减少。然而，由于缺乏关于心房颗粒内容物和确切功能的信息，我们无法得出其在阿霉素诱导的心肌病中减少具有致病意义的结论。
