营养不良仓鼠心肌细胞变性和心肌钙化的超微结构。

J A Burbach
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引用次数: 10

摘要

用电镜观察Bio 14.6型心肌病仓鼠心肌,观察心肌在急性损伤阶段细胞和细胞器的变化,这一阶段以心肌细胞破坏和钙升高为典型特征。大多数心肌细胞保持其正常的组织学和超微结构特征,但在退行性钙化病变中观察到分散的改变和坏死细胞灶。坏死前肌细胞的改变包括细胞水肿;肌浆网和t小管有不同程度的扩张;收缩带及其他肌原纤维异常;线粒体聚集和增生;线粒体的广泛变化,如大小、形状和晶体模式的改变,以及亲锇基质内含物的数量和大小的增加。在大多数改变的坏死前细胞中没有观察到与大量钙过量一致的形态学特征。相反,钙沉积在挤压的线粒体内和退化的细胞器碎片上,只有在心肌细胞破坏后才观察到。一些钙化细胞残余物被巨噬细胞吞噬,而大的钙化斑块和其他沉积物留在间质中。在高度钙化的病变中,血管平滑肌细胞和成纤维细胞的线粒体钙化很明显。这些观察结果表明,这种心肌病中存在的大多数形态学上可识别的钙沉积是由于肌层破坏后的继发性钙化所致。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Ultrastructure of cardiocyte degeneration and myocardial calcification in the dystrophic hamster.

The myocardium of the Bio 14.6 cardiomyopathic hamster was examined with the electron microscope to identify cellular and organelle changes during the acute lesioning stage, a period typified by concomitant cardiocyte destruction and calcium elevation. Most cardiocytes retained their normal histologic and ultrastructural features, but scattered foci of altered and necrotic cells were observed in association with degenerative calcifying lesions. Prenecrotic alterations of myocytes included cellular edema; varying degrees of distension of sarcoplasmic reticulum and T-tubules; contraction bands and other myofibrillar abnormalities; mitochondrial clustering and hyperplasia; a wide spectrum of mitochondrial changes such as altered sizes, shapes, and cristal patterns, and increases in the number and size of osmiophilic matrix inclusions. Morphologic features consistent with substantial calcium excess were not observed in most altered but prenecrotic cells. Instead, calcium deposition within extruded mitochondria and upon degenerating organelle debris was observed only after cardiocyte disruption. Some calcifying cell remnants were phagocytized by macrophages, whereas large calcified plaques and other deposits remained in the interstitium. Mitochondrial calcification in vascular smooth muscle cells and fibroblasts was evident in highly calcified lesions. These observations suggest that most of the morphologically identifiable calcium deposition present in this cardiomyopathy results from secondary calcification subsequent to sarcolemmal disruption.

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