摘要
目的 探讨脑动脉壁局部炎性反应、免疫反应在蛛网膜下腔出血后迟发性血管痉挛发病机制中的作用及脑池局部应用尼莫地平对迟发性血管痉挛发生的预防作用。方法 在经斜坡暴露并穿刺兔基底动脉制备蛛网膜下腔出血模型基础上 ,测量各组动物血管痉挛前、后基底动脉直径并观察血管病理变化及动脉壁免疫球蛋白IgG沉积情况。结果 存在迟发性脑血痉挛的脑动脉壁渐次出现动脉中膜平滑肌变性、坏死 ,内皮细胞脱落及外膜炎症细胞浸润等病理改变。免疫球蛋白IgG在血管壁上表现为“一过性沉积” ,与血管痉挛程度无明显关联。脑池局部应用尼莫地平在蛛网膜下腔出血后早期 ,虽然可以明显缓解脑动脉痉挛 ,但并不能完全阻止迟发性脑血管痉挛的发生。结论 本研究首次证实免疫反应仅仅参与了脑血管痉挛的发生 ,并再次证实了蛛网膜下腔出血后迟发性血管痉挛的实质是以脑动脉壁的炎性反应为主 ,为临床超早期手术清除蛛网膜下腔出血提供了理论基础。
Objective To investigate the role of immunological process and local inflammation of rabbit basilar artery in the pathogenesis of delayed vasospasm following spontaneous subarachnoid hemorrhage (SAH). In addition, local introduction of Nimodipine, a calcium channel blocker, into subarachnoid space surrounding basilar artery was evaluated as a potential treatment for cerebral vasospasm. Methods The rabbit SAH model was established through transclival approach to rabbit basilar artery (exposed and perforated). With this model, the diameter of the basilar artery was measured pre and post vasospasm. Meanwhile, the vessel pathological change and immunoglobulin(Ig) G deposition in the artery wall were observed. Results Endothelium release, degeneration and necrosis of smooth muscle cells, infiltrated external membrane with neutrophils and “transient deposition effect” of immunoglobulin(Ig) G in the wall of rabbit basilar artery after SAH were found, the latter aspect suggesting there is no close relation with the severity of vasospasm. Conclusions Our results demonstrating for the first time that immunological process only involves in the pathogenesis of cerebral vasospasm and directly support the concept that delayed vasospasm is a vasculopathy of inflammatory origin. These results further underline the importance of supraacute evacuation of blood in the subarachnoid space during clinical treatment of SAH for improving the prognosis of SAH patients.
出处
《中华神经外科杂志》
CSCD
北大核心
2001年第3期178-180,共3页
Chinese Journal of Neurosurgery
基金
黑龙江省科委资助!项目 (G97C18 4 2 )
