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实验性脑出血后高血糖致能量代谢障碍加重脑损伤的可能机制
引用本文:王小蓉,张志,李小刚.实验性脑出血后高血糖致能量代谢障碍加重脑损伤的可能机制[J].泸州医学院学报,2012,35(1):87-89.
作者姓名:王小蓉  张志  李小刚
作者单位:1. 雅安市人民医院神经内科,四川雅安,625000
2. 泸州医学院附属医院神经内科
摘    要:目的:观察大鼠脑出血(ICH)后高血糖对血肿周围脑组织含水量和三磷酸腺苷(ATP)的影响,探讨ICH后高血糖对脑损伤的可能机制。方法:采用自体血注入法建立脑出血模型,将100只SD大鼠随机分成假手术组(SO)、单纯脑出血组(PCH)、ICH后高血糖组,ICH后高血糖组又分为2g/kg(2-GS)和4g/kg(4-GS)注射葡萄糖组。观察各组大鼠术前、术后1h、6h血糖变化;测定各组大鼠术后1、3、7、10、14d血肿周围脑组织含水量和ATP含量变化。结果:与SO组比较,脑出血3组血肿周围脑组织含水量升高,ATP含量降低(P<0.05);与PCH组比较,2-GS组和4-GS组大鼠血肿周围脑组织含水量明显升高(P<0.05),ATP含量明显降低(P<0.05)。结论:提示脑出血后高血糖导致能量代谢障碍,可能通过加重脑水肿而加重脑损伤。

关 键 词:脑出血  高血糖  大鼠  三磷酸腺苷

HIGH BLOOD SUGAR EXAGGERATE BRAIN DAMAGE IN EXPERIMENTAL BRAIN HEMORRHAGE
Institution:Wang Xiaorong,et al Department of Neurology,the People’s Hospital of Ya’an
Abstract:Objective:To observe the effect of high blood glucose on water and adenosine triphosphate(ATP) content changes around hematoma in rats with intracerebral hemorrhage(ICH),and to explore its possible mechanism of brain injury.Methods:ICH model was established through autologous blood injection.100 SD rats were randomly divided into sham operation group(SO),cerebral hemorrhage group(PCH),cerebral hemorrhage plus hyperglycemia 2g/kg(2-GS) group,4g/kg(4-GS) group.Before and 1h,6h after operation blood glucose changes were observed;1,3,7,10,14d afted operation perihematoma water content and ATP levels were measured.Results: Compared with SO group,the other 3 groups with brain hemorrhage had significantly higher water content and significantly lower ATP content(P<0.05);compared with PCH group,2-IG and 4-IG group had significantly higher water content,and lower ATP content(P<0.05).ConclUSion:Hyperglycemia after cerebral hemorrhage can cause disorder of energy metabolism,and brain edema may aggravate brain damage.
Keywords:Cerebral hemorrhage  Hyperglycemia  Rats  Adenosine triphosphate
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