Pathogenesis of myonecrosis following cerebral vasospsm

脑血管痉挛后肌坏死的发病机制

• 批准号: 60570665
• 负责人: YAMASHIMA Tetsumori
• 金额: $ 0.96万
• 依托单位: University of Kanazawa
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (C)
• 财政年份: 1985
• 资助国家: 日本
• 起止时间: 1985 至 1987
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-60570665/
• 关键词: Subarachnoid hemorrhage; Meningitis; Putaminal hemorrhage; Cerebral vasospasm; Myonecrosis; Dog; Epinephrine; 電子顕微鏡; 脳血管攣縮; イヌ

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.

超微结构研究了与蛛网膜下腔出血、脑膜炎和跨脑手术相关的脑血管痉挛后肌坏死。肌坏死的基本特征是肌丝溶解，产生细颗粒或丝状物质。崩解的细胞质常含有大量的糖原颗粒、致密体、自噬液泡和髓鞘样膜体。肌丝溶解后，肌浆网发育良好，线粒体肿胀明显。细胞核呈染色质稀释或固缩改变。坏死的平滑肌细胞的基底膜明显增厚，并保持不规则的轮廓。细胞间隙增大，含有丰富的细胞碎片、泡状结构和结缔组织纤维。此外，还研究了肾上腺素注入犬交叉池后的肌坏死。镜下，威利斯细胞环显示中膜凝固坏死和纤维化。肌坏死的精细结构表现为空泡化、肌丝溶解、局灶性胞浆坏死、断裂、凝固性坏死和细胞间纤维化六个动态过程。尽管实验程序简单，但目前的模型揭示了肌坏死与人类的显著相似，并包含了先前报道的所有实验性肌坏死的超微结构特征。

项目成果

Tetsumori Yamashima: Neurosurgery. 16. 546-553 (1985)

山岛哲守：神经外科。

Tetsumori Yamashima: "Fine structure of myonecrosis following epinephrine-induced cerebral vasospasm" Neurochirurgia. 30. 29-34 (1987)

Tetsumori Yamashima：“肾上腺素引起的脑血管痉挛后肌坏死的精细结构”神经外科。

Tetsumori Yamashima: "Meningothelial rosettes in the canine subarachnoid space" Acta Neuropathologica (Berlin). 66. 223-232 (1985)

Tetsumori Yamashima：“犬蛛网膜下腔中的脑膜玫瑰花结”Acta Neuropathologica（柏林）。

Tetsumori Yamashima: Acta Neuropathologica(Berlin). 66. 223-232 (1985)

山岛哲森：神经病理学学报（柏林）。

Tetsumori Yamashima: Journal of Neurology. 233. 348-357 (1986)

山岛哲森：神经病学杂志。