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拉莫三嗪治疗脑损伤后脑水肿的实验研究 |
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程远 陈复仁 吴泳 张晓萍
【摘要】 目的 通过大鼠脑冲击伤模型,观察脑损伤后兴奋性氨基酸谷氨酸变化规律以及拉莫三嗪对急性脑水肿的治疗效果,并探讨其作用机制。方法 采用干湿重法,微透析技术及氨基酸分析测定脑损伤后不同区域,不同时相脑组织的水含量及谷氨酸的浓度。结果 (1)脑损伤组脑组织的水含量,细胞外液谷氨酸浓度明显高于对照组;(2)脑损伤组损伤区域的脑水肿和细胞外液谷氨酸呈自身扩播性;(3)拉莫三嗪治疗组脑组织含水量以及谷氨酸浓度明显低于脑损伤非治疗组。结论 拉莫三嗪通过抑制神经细胞释放谷氨酸而发挥对脑水肿的治疗作用。
【关键词】 颅脑损伤 脑水肿 兴奋性氨基酸 拉莫三嗪
Effect of Lamotrigine on Cerebral Edema Following Traumatic Brain Injury in Rats CHENG Yuan, CHEN Fu-ren, WU Yong, et al. Dept. of Neurosurgery, Second Affiliated Hospital, Chongqing Medical University, Chongqing 400042
【Abstract】 Aim To investigate the effect of lamotrigine (LTG) on cerebral edema following traumatic brain injury, and to discuss the mechanism. Methods This study was done on the experimental animal models (rats) with impacted brain injury. The change of water content in brain was measured with “drying-wet” method, and the change of glutamate was measured with microdialysis technique and amino acids automaticanalyzes. Results (1) The water content and glutamate in the injured brain were significantly greater than those in the control group. (2) In the injured brain, the contents of water and glutamate showed a self-diffusion process. (3) The contents of water and glutamate in the LTG-treated group were significantly lower than those in the nontreated group. Conclusion LTG can deal with cerebral edema by inhibiting neurons to release glutamate.
【Key words】 Brain injury Cerebral edema Excitatory amino acids Lamotrigine
脑损伤后脑组织细胞外液兴奋性氨基酸(EAA)异常增高,导致急性神经细胞肿胀和迟发性神经细胞损害已得到实验证实,并越来越引起人们重视［1］。我们通过大鼠损伤模型,应用微透析技术和氨基酸分析仪,直接对活体大鼠脑损伤后不同时相,不同区域脑组织水含量以及细胞外液的谷氨酸浓度进行测定,观察拉莫三嗪对脑组织水含量和细胞外液谷氨酸浓度的影响,并对其作用机制进行讨论。
材料与方法
一、实验动物及分组
雄性Wister大鼠,3～4月龄,体重(250±25)g,随机分三组:对照组、损伤组和治疗组。
二、急性脑损伤模型
大鼠以3%水合氯醛(1mg/kg)腹腔注射麻醉,俯位固定头部。矢状切开头皮,显露右顶骨,于人字缝前2mm、中线右旁2mm处钻孔,扩大骨窗,直径约4mm,呈“球拍”型。将撞杆头端置于骨窗硬脑膜外,用自制自由落体撞击装置,20g砝码,从20cm高处坠落,冲击撞杆,造成右顶叶局限性脑挫裂伤,治疗组于伤[1] [2] 下一页
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