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肥厚型人类心肌细胞退变变化的谱系:一项超微结构研究。

The spectrum of degenerative changes in hypertrophied human cardiac muscle cells: an ultrastructural study.

作者信息

Maron B J, Ferrans V J, Jones M

出版信息

Recent Adv Stud Cardiac Struct Metab. 1975;8:447-66.

PMID:129839
Abstract

Light and electron microscopic observations were made on cardiac tissues removed at operation from 91 patients with ventricular hypertrophy, including left ventricular myocardium from 16 patients with aortic valvular disease and from 16 patients with asymmetric septal hypertrophy, and crista supraventricularis muscle from 59 patients with congenital heart diseases associated with right ventricular outflow tract obstruction. In all patients the majority of cardiac muscle cells were hypertrophied, had intact myofibrils, and were surrounded by small amounts of fibrous tissue. In 18 (20%) of the 91 patients cardiac muscle cells with a wide spectrum of degenerative changes were present in addition to hyperthrophied, nondegenerated cells. Early degenerative changes consisted of focal myofibrillar lysis, with preferential loss of thick myofilaments, and focal proliferation of tubules of sarcoplasmic reticulum. Cardiac muscle cells with advanced degeneration had extensive myofibrillar damage and a marked decrease in numbers of myofibrils and T-tubules. The most severely degenerated cells showed selective proliferation of organelles, including sarcoplasmic reticulum, mitochondria, and glycogen, which replaced the contractile elements in the cytoplasm. These findings suggest that degenerated cardiac muscle cells have poor contractile function and may be responsible for impaired cardiac performance in some patients with ventricular hypertrophy. These morphological features appear to represent a final common pathway for degeneration of cardiac muscle cells in a variety of cardiac conditions.

摘要

对91例心室肥厚患者手术切除的心脏组织进行了光镜和电镜观察,其中包括16例主动脉瓣疾病患者和16例不对称性室间隔肥厚患者的左心室心肌,以及59例伴有右心室流出道梗阻的先天性心脏病患者的室上嵴肌。在所有患者中,大多数心肌细胞肥大,肌原纤维完整,周围有少量纤维组织。在91例患者中的18例(20%),除了肥大的、未退化的细胞外,还存在具有广泛退行性改变的心肌细胞。早期退行性改变包括局灶性肌原纤维溶解,以粗肌丝优先丢失为特征,以及肌浆网小管的局灶性增生。具有晚期退行性变的心肌细胞有广泛的肌原纤维损伤,肌原纤维和T小管数量明显减少。最严重退化的细胞表现为细胞器的选择性增生,包括肌浆网、线粒体和糖原,它们取代了细胞质中的收缩成分。这些发现表明,退化的心肌细胞收缩功能较差,可能是一些心室肥厚患者心脏功能受损的原因。这些形态学特征似乎代表了多种心脏疾病中心肌细胞退化的最终共同途径。

相似文献

1
The spectrum of degenerative changes in hypertrophied human cardiac muscle cells: an ultrastructural study.肥厚型人类心肌细胞退变变化的谱系:一项超微结构研究。
Recent Adv Stud Cardiac Struct Metab. 1975;8:447-66.
2
Ultrastructural features of degenerated cardiac muscle cells in patients with cardiac hypertrophy.心脏肥厚患者退变心肌细胞的超微结构特征
Am J Pathol. 1975 Jun;79(3):387-434.
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Myocardial ultrastructure in patients with chronic aortic valve disease.慢性主动脉瓣疾病患者的心肌超微结构
Am J Cardiol. 1975 May;35(5):725-39. doi: 10.1016/0002-9149(75)90065-x.
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[Ultrastructural changes in human myocardium with hypertrophy due to aortic valve disease and their relationship to left ventricular mass and ejection fraction (author's transl)].主动脉瓣疾病所致肥厚型人心肌超微结构变化及其与左心室质量和射血分数的关系(作者译)
Herz. 1981 Aug;6(4):217-25.
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Ultrastructure of crista supraventricularis muscle in patients with congenital heart diseases associated with right ventricular outflow tract obstruction.先天性心脏病合并右心室流出道梗阻患者室上嵴肌的超微结构
Circulation. 1975 Jan;51(1):39-67. doi: 10.1161/01.cir.51.1.39.
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Ultrastructural aspects of contractile proteins in cardiac hypertrophy and failure.心肌肥厚和心力衰竭中收缩蛋白的超微结构特征
Recent Adv Stud Cardiac Struct Metab. 1976;12:129-40.
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Left atrial ultrastructure in mitral valvular disease.二尖瓣疾病中的左心房超微结构
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Recent Adv Stud Cardiac Struct Metab. 1976;9:395-419.
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[Is secondary myocardial hypertrophy a physiological or pathological adaptive mechanism?].继发性心肌肥大是一种生理还是病理适应性机制?
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Ultrastructural features of diseased human atrial muscle cells.
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Right ventricular myocardium in Fallot's tetralogy: a light microscopic, morphometric and ultrastructural study.法洛四联症的右心室心肌:光镜、形态计量学及超微结构研究
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Cardiac disease induced by chronic adriamycin administration in dogs and an evaluation of vitamin E and selenium as cardioprotectants.
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Am J Pathol. 1980 Apr;99(1):13-42.
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Fibrillolysis and electrophoretic determination of actin and myosin in hypertrophied human myocardium.
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