实验性脑损伤超急性期脑糖代谢的变化  

Cerebral glucose metabolism study of early acute experimental brain inijury in rabbits

作　　者：胡卫星[1] 顾培元[1] 吴幼章[1] 付震[1] 马剑峰[1] 颜承靖[1] 张家明 

机构地区：[1]南京医科大学第一附属医院,210029

出　　处：《中华实验外科杂志》1998年第6期553-554,共2页Chinese Journal of Experimental Surgery

基　　金：卫生部青年自然科学基金(No:93214))

摘　　要：目的探讨脑损伤后急性期脑糖代谢变化的病理过程及其机理。方法自由落体法建立兔右侧大脑半球脑外伤模型,于伤前及伤后15′、30′、2小时和24小时分别取动脉和双侧颈静脉球血样,监测其血糖及胰岛素、胰高血糖素、皮质醇、ACTH。结果脑损伤后受伤侧大脑半球即发生糖代谢下降,耗糖量自伤前1.5908±0.99下降到0.5062±0.64(P<0.01),而对侧半球在受伤侧致伤后2小时内糖代谢仍维持正常(P>0.05),24小时耗糖明显下降(P<0.01)。伤后胰高血糖素极度持续增高,胰岛素无明显变化。结论脑损伤后糖代谢障碍自受伤局部发生、发展而累及对侧半球。胰高血糖素极度增高及胰岛素与胰高血糖素的比例失衡使体循环血糖明显升高。Objective To detect the pathological process and pathogenesis of brain glucose metabolism follow-ing acute brain injury. Methods The brain injuy models were established by the method described by Young. The blood samples were collected from femoral artery and both jugular bulbs before brain injury and at 15 rain, 30 man, 2 h and 24 h after injury, respectively. Blood glucose, insulin, glucagon, cortisol, and ACTH in blood were measured. Results After brain injury,the glucose metabolism consumption was immediately affected in the injured cerebral hemisphere, decreased from 1. 5908±0. 99 pre-injury to0. 5062±0. 6 (P<0. 01) post-injury. However, in the contralateral (normal) hemisphere, glucose metabolism consumption was still normal in the 2 h after right hemisphere injured (P<0. 05). After brain injury, geucagon was extremely increased and insulin retained normally. Conclusion The glucose metabolism disturbance in the injured brain aggravated in the injured part and invaded into the whole brain. The increase of blood glucose in the systemic circulation was resulted from the elevation of glucagon and the disorder of insulin/glucagon.

关 键 词：糖代谢 胰高血糖素 胰岛素 颅脑损伤 兔 

分 类 号：R651.150.2[医药卫生—外科学]