Ultrastructural alterations of atrial myocardium induced by adriamycin in chronically treated animals.
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.
D000818:Animals; D004317:Doxorubicin / Q000633:toxicity*; D006321:Heart / Q000187:drug effects*; D006325:Heart Atria / Q000187:drug effects; D006352:Heart Ventricles / Q000187:drug effects; D006801:Humans; D051379:Mice; D008929:Mitochondria, Heart / Q000187:drug effects; D009205:Myocarditis / Q000139:chemically induced* / Q000473:pathology; D009206:Myocardium / Q000378:metabolism / Q000648:ultrastructure*; D009210:Myofibrils / Q000187:drug effects; D011817:Rabbits; D012261:Ribonucleoproteins / Q000378:metabolism; D012519:Sarcoplasmic Reticulum / Q000187:drug effects
D012261:Ribonucleoproteins; D004317:Doxorubicin