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应用家免失血性休克模型观察心肌的超微结构改变。结果发现(1)间盘两侧的心肌纤维呈区带性病变,肌膜呈扇形膨出;Z带互相靠近,肌节缩短;Z带断裂,肌原纤维走向紊乱;线粒体移位至距间盘较远的地区;(2)间盘区以外广大地区心肌纤维显示细胞内水肿;线粒体肿胀,脊破坏减少;肌原纤维灶性溶解;肌浆网小管稀少、断离、扩张及囊泡化等改变。这些改变使心肌的供能装置、收缩结构以及兴奋收缩偶联过程遭到破坏,妨碍心肌收缩功能,从而构成并发急性心功能不全的超微结构基础。
Application of home-free hemorrhagic shock model to observe myocardial ultrastructural changes. The results showed that: (1) Myocardial fibers on both sides of the intervertebral disc showed zonal lesions with fan-shaped bulges of the sarcolemma; Z bands were close to each other and the sarcomeres were shortened; Z band was disrupted and myofibrils were disordered; (2) Myocardial fibers in extensive areas outside the interplate area show intracellular edema; swelling of mitochondria, reduction of ridge destruction; focal fibrolysis of myofibrils; rare, detached, dilated and vesicular Change. These changes undermine the cardiac energy supply device, contractile structure and excitatory contractile coupling process, hinder myocardial contractile function, which constitutes the basis of the ultrastructure of acute cardiac insufficiency.