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作 者:胡卫星[1] 顾培元[1] 吴幼章[1] 傅震[1] 马剑峰[2] 颜承靖[2] 张家明
机构地区:[1]南京医科大学第一附属医院神经外科,210029 [2]南京医科大学第一附属医院检验科,210029
出 处:《江苏医药》1998年第11期785-787,共3页Jiangsu Medical Journal
基 金:卫生部青年科学研究基金
摘 要:以免脑损伤模型为基础,通过监测糖代谢激素及脑动静脉血糖的变化探讨脑损伤后脑糖代谢的改变。脑损伤后胰高血糖素、皮质醇和ACTH持续极度增高,而胰岛素无明显变化;伤后30分钟与2小时、24小时动脉血糖升高,与伤前比较P<0.05和P<0.01。伤后受伤侧大脑半球即发生耗糖量下降,与伤前比较伤后各时相P均<0.01;而对侧半球在受伤倒致伤后2小时内耗糖仍维持正常,24小时下降(P<0.05)。伤后脑糖代谢障碍自受伤局部发生、发展而累及对侧半球。This paper focused on the alterations of cerebral glucose metabolism after brain injury. The glucose metabolism hormones and cerebral arterial blood and cerebral venous blood glucose were monitored in the rabbit after acute brain injury in different periods. After brain injury, glucagon, cortisol, ACTH increased extremely high in blood. However, insulin retained in normal level. The arterial blood glucose increased obviously 30min(P<0. 05), 2hr and 24hr (P values less than 0. 01) after injury in comparing with that of pre-brain injury. The glucose consumption was immediately affected in the injured cerebral hemisphere. The glucose consumptions decreased remarkably 30min, 2hr and 24hr after brain injury, all P values were less than 0. 01 in comparing with that of pre-injury glucose consumption. Meanwhile it was still normal in the contralateral hemisphere in 2hr (P>0.05) after injury and then became reduced 24hr later (P<0. 05). This glucose metabolism fault happened in the injured brain first and later invaded the whole brain, resulting in brain dysfunction.
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