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机构地区:[1]第二军医大学长征医院神经外科
出 处:《第二军医大学学报》1996年第3期233-235,共3页Academic Journal of Second Military Medical University
摘 要:目的:探讨兴奋性氨基酸对创伤性脑水肿的影响及作用机理。才法:在已建立的猫创伤性脑水肿模型基础上,伤后20min小脑延髓地内注入谷氨酸单钠溶液,伤后6h测定两侧大脑半球脑含水量及阳离子含量变化。结果:与对照组比较,脑含水量及Na+,Ca2+含量明显增加;K+,Mg2+含量则相应降低,这种变化具有剂量依赖性。结论:谷氨酸有加重创伤性脑水肿的作用,谷氨酸使Na+和Ca2+内流增加可能是其加重脑水肿的主要病理生理机理。To evaluate the effect and mechanism of excitatory amino acids on traumatic brain edema.Methods: Using a established model of traumatic brain edema in cats, we injected the solutions of sodium glutamate into cerebellomedullary cistern of cats 20 min post-traumatic brain injury and measured the contents of brain tissue water, cation in the bilateral cerebral hemispheres 6 h posti-njury. Results: There were significant increases in the contents of brain tissue water , Na ̄+ and Ca2 ̄+, whereas there were marked decreases in the contents of brain K ̄+ and Mg ̄2+ as compared with the control group. The changes above were dose-dependent.Conclusion : Glutamate may contribute to traumatic brain edema. The increases of Na ̄+ and Ca ̄2+ influx may be the main pathophysiological mechanism of glutamate in exacerbating brain edema post-injury.
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