目的观察在缺血性脑卒中发生后,高血糖对脑糖水平及脑卒中损伤的影响.方法:采用线栓栓塞大脑中动脉诱发大脑局灶性脑缺血模型模拟缺血性脑卒中,在再灌注前5 min 单次腹腔注射50% 葡萄糖溶液(6 mL·kg^-1)诱导再灌注早期高血糖.在再灌注30 min 和24 h 时检测脑糖水平,并通过神经功能评分及脑梗死面积的统计评价脑缺血再灌注损伤.结果:给予葡萄糖后,血糖显著增加,并持续至再灌注后120 min( P〈0.05).缺血再灌注损伤可引起脑糖水平的增加,再灌注早期血糖的升高会进一步加重再灌注24 h 时脑糖水平的增加,并显著增加再灌注24 h 时神经功能评分和脑梗死面积(P〈0.05).结论:脑缺血后,再灌注早期高血糖可加重再灌注后脑糖水平和脑损伤的增加,脑糖水平的升高可能是高血糖介导的脑卒中损伤加重的直接原因.
[ABSTRACT]Objective:To explore the effects of hyperglycemia on cerebral glucose level and brain injury after ischemic stroke.Methods:The middle cerebral artery occlusion(MCAO) model was used to mimic the ischemic stroke. Hyperglycemia in acute reperfusion was induced by single intraperitoneal injection of 50% glucose(6 mL·kg-1) at 5 min before reperfusion in MCAO-treated rats. After reperfusion for 30 min and 24 h,the cerebral glucose levels were detected,and the neurological score and infarct areas were assessed.Results:After glucose administration,the blood glucose increased significantly and lasted for 120 min after reperfusion (P<0.05). Ischemia and reperfusion injury caused cerebral glucose increase. Hyperglycemia in acute reperfusion significantly aggravated the elevation of cerebral glucose,and increased the neurological scores and infarct areas after reperfusion for 24 h(P<0.05).Conclusion:After cerebral ischemia,hyperglycemia in acute reperfusion could aggravate cerebral glucose increase and stroke injury. The elevation of cerebral glucose levels might directly mediate aggravation of stroke injury caused by hyperglycemia.