IMPAIRMENT OF THE MYOCARDIAL ULTRASTRUCTURE AND CHANGES OF THE CYTOSKELETON IN DILATED CARDIOMYOPATHY
IMPAIRMENT OF THE MYOCARDIAL ULTRASTRUCTURE AND CHANGES OF THE CYTOSKELETON IN DILATED CARDIOMYOPATHY
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DOI：
10.1161/01.cir.83.2.504
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发表时间：
1991-02-01
期刊：
影响因子：
37.8
通讯作者：
BLEESE, N
中科院分区：
文献类型：
--
作者：
SCHAPER, J;FROEDE, R;BLEESE, N
本研究旨在确定慢性心力衰竭的形态学相关性。8例因终末期扩张型心肌病接受移植手术的患者的心肌组织通过电子显微镜和免疫细胞化学进行了研究，使用单克隆抗体对细胞骨架的元素：结蛋白，微管蛋白，黏着斑蛋白和波形蛋白。组织显示肥大、肌细胞萎缩和纤维化量增加。超微结构变化包括细胞核增大和形状变化，大量非常小的线粒体，T小管增生，脂滴和糖原积聚。最明显的超微结构改变是肌丝减少，从稀疏到充满未指明细胞质的细胞中完全没有肌节。免疫细胞化学显示结蛋白定位于Z线。病变心肌结蛋白含量增加，但排列紊乱。微管蛋白在整个心肌细胞中形成精细的网络，并且在心肌病心脏中显著增加。与细胞骨架密切相关的蛋白质，不仅存在于肌膜和闰盘，而且也存在于心肌细胞内。约三分之一的细胞超微结构变化和细胞骨架的改变是严重的。大约三分之一的细胞显示出中度严重的变化，其余细胞正常。波形蛋白存在于间质细胞中，并且随着纤维化的增加而增加。我们的结论是纤维化的增加，肥大的心肌细胞的变性，和细胞骨架的改变是慢性心力衰竭心肌功能下降的形态学相关性。
This study was designed to determine the morphological correlate of chronic heart failure. Myocardial tissue from eight patients undergoing transplantation surgery because of end-stage dilated cardiomyopathy was investigated by electron microscopy and immunocytochemistry using monoclonal antibodies against elements of the cytoskeleton: desmin, tubulin, vinculin, and vimentin. The tissue showed hypertrophy, atrophy of myocytes, and an increased amount of fibrosis. Ultrastructural changes consisted of enlargement and varying shape of nuclei, numerous very small mitochondria, proliferation of T tubules, and accumulation of lipid droplets and glycogen. The most obvious ultrastructural alteration was the decrease of myofilaments, ranging from rarefication to complete absence of sarcomeres in cells filled with unspecified cytoplasm. Immunocytochemistry showed that desmin was localized at the Z lines. In diseased myocardium, the amount of desmin was increased, but it was disorderly arranged. Tubulin formed a fine network throughout the myocytes and was significantly increased in cardiomyopathic hearts. Vinculin, a protein closely associated with the cytoskeleton, occurred not only at the sarcolemma and the intercalated disc but also within the myocardial cells. Ultrastructural changes and alterations of the cytoskeleton were severe in about one third of all cells. About one third of all cells showed moderately severe changes, and the remaining cells were normal. Vimentin was present in the interstitial cells and was increased in relation to the increase of fibrosis. We conclude that the increase of fibrosis, the degeneration of hypertrophied myocardial cells, and the alterations of the cytoskeleton are the morphological correlates of reduced myocardial function in chronic heart failure.