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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 investigate the pathological process and mechanism of brain glucose metabolism in acute phase after brain injury. Methods The left hemisphere traumatic brain injury models were established by free-fall method. Arterial and bilateral jugular bulb blood samples were taken before and 15, 30, 2 and 24 hours after injury respectively. The blood glucose, insulin, Glucagon, Cortisol, ACTH. Results The hemiplegia of the injured side of the injured brain caused a decrease of glucose metabolism. The amount of sugar consumption dropped from 1.5908 ± 0.99 to 0.5062 ± 0.64 (P <0.01), while the contralateral hemisphere was still within 2 hours after injury Normal maintenance (P> 0.05), 24 hours after consumption of glucose decreased significantly (P <0.01). Post-traumatic glucagon extremely sustained increase in insulin no significant change. Conclusion After glucose-induced brain injury, dysfunctions occur locally and develop in the contralateral hemisphere. Glucagon extreme increase in insulin and glucagon ratio imbalance so that systemic blood glucose was significantly increased.