Pathogenesis of myonecrosis following cerebral vasospsm

对蛛网膜下腔出血、脑膜炎和侧裂手术引起的脑血管痉挛后肌坏死进行了超微结构研究。肌坏死的基本特征是肌丝溶解，形成细颗粒状或丝状物质。崩解的细胞质中含有大量糖原颗粒、致密体、自噬空泡和髓鞘样膜体。尽管肌丝溶解，但发育良好的肌浆网得以保留，而线粒体显示出明显的肿胀。细胞核染色质稀释或固缩。基底膜明显增厚，坏死的平滑肌细胞轮廓不规则。增大的细胞间隙含有丰富的细胞碎片、泡状结构和结缔组织纤维。此外，对犬视交叉池注射肾上腺素后的肌坏死进行了研究。显微镜下Willis环呈凝固性坏死，中膜纤维化。肌坏死的超微结构表现为空泡化、肌丝溶解、灶性胞浆坏死、碎裂、凝固性坏死和细胞间纤维化6种动态变化。尽管一个简单的实验程序，本模型揭示了肌坏死与人类有显着的相似性，并包含所有以前报道的实验性肌坏死的超微结构特征。

Myonecrosis following cerebral vasospasm associated with subarachnoid hemorrhage, meningitsis and trans-sylvian surgery was ultrastructurally studied. The basic feature of myonecrosis was dissolution of myofilaments with resultant fine granular or filamentous material. The disintegrating cytoplasm often contained numerous glycogen granules, dense bodies, autophagic vacuoles and myelin-like membranous bodies. A well-developed sarcoplasmic reticulum was preserved despite myofilament dissolution, while mitochondria showed marked swelling. The nuclei showed either dilution of chromatin or pyknotic change. The basal lamina was remarkably thickened and maintained an irregular outline of the necrotic smooth muscle cells. Enlarged intercellular space contained abundant cellular debris, vesicular structures and connective tissue fibers. Furthermore, myonecrosis following the injection of epinephrine into the canine chiasmatic cistern was studied. Microscopically, the circle of Willis showed coagulation necrosis and fibrosis of the media. The fine structure of myonecrosis was characterized by six dynamic chenges of vacuolation, dissolution of myofilaments, focal cytoplasmic necrosis, fragmentation, coagulation necrosis and intercellular fibrosis. Despite a simple experimental procedure, the present models disclosed myonecrosis with a marked similarity to humans and contained all of the previously reported ultrstructural features of experimental myonecrosis.