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部分耳廓的半固定会诱导心肌细胞肥大和超微结构改变。

A semi-immobilization of a partial auricle induces hypertrophy and ultrastructural alteration of cardiomyocytes.

作者信息

Muto M, Wakao Y, Morimoto M, Klomkleaw W, Fuller G A, Nakayama T, Oba T, Kasashima Y, Hamlin R L, Yamaguchi M

机构信息

Department of Veterinary Surgery, Azabu University, Kanagawa, Japan.

出版信息

Int J Cardiol. 2001 Dec;81(2-3):189-99. doi: 10.1016/s0167-5273(01)00566-6.

Abstract

Semi-immobilization of a partial area of the ventral edge, lateral epicardium of the left auricle (ventrolateral of left auricle), by using quick adhesion glue induces moderate hypertrophy of myocytes with an average increase of 34% in cross-sectional area. Intercellular connective tissues increased, and cellular sizes varied markedly. The ultrastructure of immobilized (semi-immobilized) myocytes commonly exhibited degenerating features in myofibrils, various cytoplasmic organelles including mitochondrial cristae and sarcoplasmic reticulum (SR) were disrupted, and T-tubules disappeared. Z-line streaming and widening (hypertrophic Z-line, rod bodies) and increase of metabolic particle deposition are typical phenomena in addition to intercalated disc (Id) disorganization. The results suggest that semi-immobilization of the auricle induces hypertrophy of myocytes in association with degeneration and disruption of myofibrils and other cytoplasmic organelles, and an increase of intercellular connective tissues, rather than increase of myofibril mass. This is the first study to immobilize only a part of the heart rather than the whole animal. Our results using artificial immobilization of cardiac myocytes were extremely significant since the structural alterations obtained were similar to that observed in cardiomyopathies. This suggests that myocytes progressing to heart failure are also subjected to inhibition of movement. Therefore, this experiment may prove very useful as a model for studying the functional effect of heart failure observed in cardiomyopathy.

摘要

使用速粘胶对腹侧边缘部分区域(左耳外侧心外膜,即左耳腹外侧)进行半固定,可诱导心肌细胞中度肥大,横截面积平均增加34%。细胞间结缔组织增加,细胞大小差异明显。固定(半固定)心肌细胞的超微结构通常显示肌原纤维出现退化特征,包括线粒体嵴和肌浆网(SR)在内的各种细胞质细胞器被破坏,T小管消失。除闰盘(Id)紊乱外,Z线流注和增宽(肥大的Z线、杆状体)以及代谢颗粒沉积增加是典型现象。结果表明,耳廓半固定诱导心肌细胞肥大,同时伴有肌原纤维和其他细胞质细胞器的退化和破坏,以及细胞间结缔组织增加,而非肌原纤维质量增加。这是首次仅对心脏的一部分而非整个动物进行固定的研究。我们使用人工固定心肌细胞的结果非常重要,因为所获得的结构改变与心肌病中观察到的相似。这表明进展为心力衰竭的心肌细胞也受到运动抑制。因此,该实验作为研究心肌病中观察到的心力衰竭功能效应的模型可能非常有用。

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