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背景:蛛网膜下腔出血(SAH)后脑血管痉挛(CVS)是引起SAH致死和致残的主要原因,其发病机制目前还不要十分清楚。既往临床及实验研究均提示中药在某种程度上可改变SAH后脑血流变性质,改善脑功能。目的:探讨活血化瘀中药(HXHY)脑伤泰对大鼠蛛网膜下腔出血(SAH)后脑血管痉挛(CVS)后脑血流量(rCBF)及脑微血管构筑等方面的影响及其作用机制。设计:随机对照的试验。单位:解放军第三军医大学西南医院神经外科,解放军第四军医大学西京医院全军神经外科研究所。材料:实验在第三军医大学西南医院神经外科实验室和第三军医大学基础部中心实验室完成。选用288只雄性Wistar大鼠。方法:通过大鼠枕大池自体血注入法制备SAH和CVS模型,并在1,4,12,24h,3,7,14d及21d等不同时相点,观测各组大鼠局部rCBF、病理变化、脑微血管构筑和BBB超微结构变化。主要观察指标:①大鼠皮质rCBF变化。②脑光镜下病理改变。③脑皮质微血管构筑。④BBB的超微变化。结果:SAH后大鼠的rCBF、病理变化、脑微血管构筑和BBB超微结构变化的动态变化符合CVS的发展规律,HXHY和尼莫地平(Nim)对上述改变有不同程度的改善。结论:SAH后局部rCBF的变化可可以反映该时期CVS的状态,HXHY和Nim可通过多种机制对CVS发挥作用,其中“细胞保护”作用可能更为重要。
BACKGROUND: Cerebral vasospasm (CVS) after subarachnoid hemorrhage (SAH) is the main cause of death and disability of SAH. The pathogenesis of SAH is still not clear. Previous clinical and experimental studies have suggested that Chinese medicine can, to some extent, change the rheological properties of cerebral blood after SAH and improve brain function. OBJECTIVE: To investigate the effect and mechanism of blood circulation and blood stasis Chinese medicine (HXHY) brain injury Thai on cerebral blood flow (rCBF) and cerebral microvascular architecture after subarachnoid hemorrhage (SAH) in rats. Design: Randomized controlled trials. Unit: Department of Neurosurgery, Southwest Hospital, Third Military Medical University, PLA, Institute of Neurosurgery, Xijing Hospital, Fourth Military Medical University, PLA. MATERIALS: Experiments were performed at the Department of Neurosurgery, Southwest Hospital, Third Military Medical University and the Central Laboratory of the Third Military Medical University. 288 male Wistar rats were used. METHODS: SAH and CVS models were prepared by injection of autologous blood into the occipital cistern of rats. The local rCBF and pathological changes were observed at 1, 4, 12, 24, 3, 7, 14 and 21 days. , brain microvascular architecture and BBB ultrastructural changes. MAIN OUTCOME MEASURES: 1 Changes in rCBF in rat cortex. 2 brain light pathological changes. 3 cerebral cortex microvascular architecture. 4BBB’s ultra-fine changes. RESULTS: The changes of rCBF, pathological changes, brain microvessel construction and BBB ultrastructural changes in rats following SAH were in line with the development of CVS. HXHY and nimodipine (Nim) improved the above changes to varying degrees. Conclusion: The change of local rCBF after SAH can reflect the state of CVS during this period. HXHY and Nim can play a role in CVS through a variety of mechanisms, among which “cytoprotection” may be more important.