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机构地区:[1]南昌大学第一附属医院神经外科,330006 [2]武警江西总队医院神经外科
出 处:《中华神经外科杂志》2008年第8期589-592,共4页Chinese Journal of Neurosurgery
基 金:国家自然基金资助项目(39960076)
摘 要:目的探讨缝隙连接抑制剂甘珀酸对实验性蛛网膜下腔出血后脑血管痉挛的治疗作用。方法建立兔蛛网膜下腔二次出血模型,脑池及静脉分别给与缝隙连接抑制剂甘珀酸,脑血管造影及光镜观察分析基底动脉的直径及形态学变化,并应用Western blotting检测基底动脉Cx43蛋白的表达变化。结果给与甘珀酸后,基底动脉狭窄程度及光镜下形态学变化显著减轻:单纯注血组(65.7±10.3)%,脑池处理组(91.2±6.4)%,静脉处理组(96.4±11.0)%,脑池预处理组(89.7±12.8)%;同时也显著抑制了痉挛后Cx43蛋白表达水平的升高:单纯注血组(57.2±2.8)%,脑池处理组(10.0±5.3)%,静脉处理组(15.2±1.7)%。结论缝隙连接抑制剂甘珀酸可能对蛛网膜下腔出血后脑血管痉挛起到预防和治疗作用。Objective The study was designed to investigate the role of gap junctions in the pathogenesis of cerebral vasospasm after experimental subarachnoid hemorrhage (SAH). Methods We used the double-hemorrhage model of SAH with injection of autologous arterial blood into the cisterna magna. Carbenoxolone was given intracisternally or intravenously. Angiography and hematoxylin and eosin staining were performed to observe the diameter and for morphological study of the basilar artery. Western blotting was used to analyze the expression change of Cx43 protein in basilar artery. Results After the injection of carbenoxolone, arterial narrowing and morphological changes in vascular structure were significantly less than those in SAH-only group and vehicle groups; Western blotting showed that carbenoxolone could down- regulated Cx43 protein expression. Conclusions Gap junction inhibitor can attenuate cerebral vasospasm after SAH in rabbits in vivo.
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