Nagata K, Sasaki T, Mori T, Nikaido H, Kobayashi E, Kim P, Kirino T
Department of Neurosurgery, Showa General Hospital, Tokyo, Japan.
Surg Neurol. 1996 May;45(5):442-7. doi: 10.1016/0090-3019(95)00455-6.
The possible role of inflammation in the pathogenesis of cerebral vasospasm has been noted in recent studies. In order to examine the role of inflammation, we examined the vasocontractile activity of talc, which is known to cause severe inflammation, using a canine cisternal talc injection model.
Under general anesthesia, a sterile talc powder suspended in saline was injected into the cisterna magna of the dog. Serial vertebral angiography and postmortem histologic changes of the harvested basilar artery were examined. The morphologic and pharmacologic features of talc-induced vessel spasm were compared with the usual autologous blood-induced artery spasm.
Cisternal injection of sterile talc powder caused no early spasm, but induced definite basilar arterial constriction 2 days after injection. This vascular constriction was observed to continue up to 7 days after injection. Ultrastructural study of the constricted vessel revealed several morphologic changes, such as corrugation of the elastic lamina, subintimal proliferation, migration of smooth muscle cells, detachment of endothelial cells, etc.; findings that are compatible with the changes observed in vasospasm. Pharmacologic study showed a moderate decrease in the maximal contraction to KCl and UTP. Endothelium-dependent relaxation was markedly disturbed, while endothelium-independent relaxation was preserved. These pharmacologic properties were also similar to those reported in vasospasm.
Our present study indicates that the several changes of vascular properties, which had been considered to be specific to cerebral vasospasm, can be regarded as a nonspecific biologic defense reaction against the foreign body. The analysis of the common pathway from talc and autologous blood to vasospasm may lead to the pathogenesis of cerebral vasospasm.
近期研究已注意到炎症在脑血管痉挛发病机制中可能发挥的作用。为研究炎症的作用，我们使用犬枕大池注射滑石粉模型，检测了已知可引发严重炎症的滑石粉的血管收缩活性。
在全身麻醉下，将悬浮于生理盐水中的无菌滑石粉注入犬的枕大池。对采集的基底动脉进行系列椎动脉血管造影及死后组织学变化检查。将滑石粉诱导的血管痉挛的形态学和药理学特征与常见的自体血诱导的动脉痉挛进行比较。
枕大池注射无菌滑石粉未引起早期痉挛，但在注射后2天诱发了明确的基底动脉收缩。观察到这种血管收缩在注射后持续长达7天。对收缩血管的超微结构研究显示了一些形态学变化，如弹性膜皱缩、内膜下增殖、平滑肌细胞迁移、内皮细胞脱落等；这些发现与血管痉挛中观察到的变化一致。药理学研究表明，对氯化钾和三磷酸尿苷的最大收缩反应适度降低。内皮依赖性舒张明显受损，而非内皮依赖性舒张则得以保留。这些药理学特性也与血管痉挛中报道的特性相似。
我们目前的研究表明，曾被认为是脑血管痉挛特有的几种血管特性变化，可被视为针对异物的非特异性生物防御反应。对滑石粉和自体血至血管痉挛的共同途径的分析可能会揭示脑血管痉挛的发病机制。
