Pathogenesis of myonecrosis following cerebral vasospsm

对蛛网膜下腔出血、脑膜炎和经侧突入路手术所致的脑血管痉挛所致的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，形成细小颗粒状或丝状物质。崩解的细胞质中常含有大量糖原颗粒、致密小体、自噬空泡和髓磷脂样膜小体。尽管肌丝溶解，但仍保留了发达的肌浆网，而线粒体则明显肿胀。核染色质稀疏或固缩改变。基底板明显增厚，并保持不规则的坏死性平滑肌细胞轮廓。扩大的细胞间隙内含有丰富的细胞碎片、泡状结构和结缔组织纤维。此外，我们还研究了犬交叉脑池注射肾上腺素后的心肌坏死。镜下见Willis环可见中膜凝固性坏死和纤维化。心肌坏死的细微结构以空泡化、肌丝溶解、局灶性胞浆坏死、碎裂、凝固性坏死和细胞间纤维化6种动态改变为特征。尽管实验过程简单，但本模型揭示的心肌坏死与人类有显著的相似之处，并包含了先前报道的实验性心肌坏死的所有超微结构特征。

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.