主动脉不完全结扎慢性实验性心力衰竭的超微结构研究

Ultrastructural Investigation of Eailing Myocardium in Experimental Animals

本文建立了一种主动脉不完全结扎慢性心力衰竭的动物模型,并研究了其超微结构变化。慢性心力衰竭的心肌存在不同类型的心肌细胞变性:(一)严重变性的心肌细胞胞质内充满增生的线粒体,肌原纤维被取代;(二)变性细胞中大片肌原纤维溶解,肌浆网小管和小泡增殖,粗面内质网丰富,溶酶体活跃;(三)变性细胞肌原纤维完整而线粒体全部被溶酶体自噬破坏。与此同时,还经常观察到线粒体灶性增生、肌原纤维灶性溶解以及走向紊乱等局灶变性改变。结果表明:心肌细胞的肌原纤维和线粒体破坏导致心肌收缩性障碍,可能是心力衰竭发生的重要机制。

Animal model of chronic cardiac failure induced by abdominal aortic stenosis was utilized to charaterize the ultrastructural changes of chronic cardiac failure. There were several kinds of severe degenerated cardiac muscle cells: one was entirelly filled with hyperplastic mitochondria replacing myofilaments in the cytoplasm; another appeared myofibrillar lysis in large areas of the cytoplasm and contained increased numbers of tubules as well as cisterns of sarcoplasmic reticulum; the last one was observed that their mitochondria were digested bylysosomes and the myofibrillae were not injured. Simullaneously, there were many foci of cardiac myocyte dam-age, such as focal mitochondrial hyperplasia, myofibrillar lysis and myofibrillar disarray and so on. The findings of present study indicated that: it may be the important mechanism of cardiac failure that myofibrillar andmitochondrial disruption resulted in obstacle of myocardial contractivility.