摘要
本文在大鼠双侧颈总动脉闭塞的不完全性脑缺血模型上,观察了高血糖对脑缺血的作用。结果表明高血糖能增加缺血动物死亡率及存活动物的神经缺陷积分,加剧缺血性脑水肿并干扰了缺血时rCBF的恢复。对高血糖加剧脑缺血性损伤的病理机制进行了讨论。
We compared the effects of glucose injection with those of saline on Wistar rats undergoimg 24 hours occlusion of both common carotid arteries. The mortality, neurological deficit score and brain water content in hyperglycemic group were signffcantly higher than those in normoglycemic group (P<0.01). 24 hours after ischemia, there was a delayed hypoperfusion in hyperglycemic group. Pathological study demonstrated that hyperglycemia markedly augmented morphologic brain damage. We conclude that hyperglycemia can excerbate cerebral ischemia in rats and its possible mechanism may be due to the accumulation of lactic acid in the ischemic brain.
出处
《临床神经病学杂志》
CAS
1992年第1期25-27,共3页
Journal of Clinical Neurology