Hatt P Y
Recent Adv Stud Cardiac Struct Metab. 1975;6:325-33.
The electron microscopic aspects of myocardial cells in several types of mechanically overloaded heart are reviewed. Alterations which may be interpreted as degenerative changes are all the more frequent as the load is more severe. They seem to be the cause of the interstitial fibrosis which often accompanies hypertrophy. Their mechanism is dubious: swelling of mitochondria and intracellular lipidosis, which could signify cellular hypoxia, are rarely present. Other changes are characteristic of an increase of proteosynthesis and of the active growth of the main structures of the cell: myofibrils, mitochondria, T- and L-tubules. Some pictures of myofibrillar growth are not always easily distinguished from those of myofibrillar lesions. The mitochondria/myofibril ratio may be modified or not. The apparent volume of the mitochondria may remain normal while their density increases, which implies a decrease of their average size. In severe and long-lasting overloads, hypertrophy and hyperplasia of the Golgi apparatus and multiplication of granules of the auricular type evoke a regression of the cell toward its fetal type.
本文综述了几种机械性负荷过重心脏中心肌细胞的电子显微镜观察结果。随着负荷加重，可被解释为退行性改变的变化更为频繁。它们似乎是常伴随肥大出现的间质纤维化的原因。其机制尚不清楚：很少出现可提示细胞缺氧的线粒体肿胀和细胞内脂质沉积。其他变化是蛋白质合成增加以及细胞主要结构（肌原纤维、线粒体、T小管和L小管）活跃生长的特征。一些肌原纤维生长的图像并不总是容易与肌原纤维损伤的图像区分开来。线粒体/肌原纤维的比例可能改变，也可能不变。线粒体的表观体积可能保持正常，但其密度增加，这意味着其平均大小减小。在严重且持久的负荷过重情况下，高尔基体的肥大和增生以及心房型颗粒的增多会使细胞向胎儿型退化。
