Van Vleet J F, Ferrans V J
Am J Vet Res. 1982 Nov;43(11):2000-9.
Seventy newly hatched ducklings were fed a commercial ration with 500 mg of added Te (as tetrachloride)/kg of feed for up to 28 days. Ducklings were euthanatized at day 14, 21, and 28, the hearts were studied by gross, microscopic, and ultrastructural examination. Cardiac damage was apparent grossly as hydropericardium and myocardial hemorrhage. Histopathologically, the ventricular myocardium had areas of acute hemorrhagic necrosis (often with mineralization), edema, and congestion. Resolving areas of necrosis appeared cellular with macrophages, heterophils, fibroblasts, and pale vacuolated cells with large vesicular nuclei that were identified as dedifferentiated myocytes. Ultrastructurally, necrotic fibers had disrupted contractile material and mineralized mitochondria. In resolving lesions, macrophages were numerous in the interstitium and within necrotic fibers. Also, a population of sublethally injured myocytes was present and appeared as dedifferentiated cardiac muscle cells with few myofibrils, scattered free filaments, prominent sarcoplasmic reticulum, abundant glycogen, and large nuclei with prominent nucleoli. These dedifferentiated myocytes represented a reparative phase of the Te-induced myocardial injury which has been termed "reactive hyperplasia" and "rejuvenating reorganization" in previous models of myocardial damage.
70只刚孵出的小鸭被喂食添加了500毫克碲（以四氯化物形式）/千克饲料的商业日粮，持续28天。在第14天、21天和28天对小鸭实施安乐死，通过大体、显微镜和超微结构检查对心脏进行研究。心脏损伤在大体上表现为心包积水和心肌出血。组织病理学上，心室心肌出现急性出血性坏死区域（常伴有矿化）、水肿和充血。正在消退的坏死区域可见含有巨噬细胞、嗜异性粒细胞、成纤维细胞的细胞，以及具有大泡状核的淡染空泡化细胞，这些细胞被鉴定为去分化的心肌细胞。超微结构上，坏死纤维的收缩物质遭到破坏，线粒体发生矿化。在正在消退的病变中，间质和坏死纤维内巨噬细胞数量众多。此外，还存在一群亚致死性损伤的心肌细胞，表现为去分化的心肌细胞，肌原纤维少，游离细丝散在分布，肌浆网突出，糖原丰富，细胞核大且核仁明显。这些去分化的心肌细胞代表了碲诱导的心肌损伤的修复阶段，在先前的心肌损伤模型中这一阶段被称为“反应性增生”和“再生性重组”。
