目的：探讨缺氧缺血性脑损伤(H IBD)后脑内负责葡萄糖转运的两个重要蛋白质葡萄糖转运蛋白-1(GLUT-1)与葡萄糖转运蛋白-3(GLUT-3)表达的变化,揭示H IBD后脑内能量衰竭的发病机制。方法：将30只7日龄W istar大鼠随机分为正常对照组(n=5)、假手术对照组(n=5)和H IBD组(n=20)。H IBD组大鼠模型的制备参照R ice。方法结扎右侧颈总动脉后8%低氧暴露1 h。假手术对照组只分离右侧颈动脉,不予结扎和缺氧。缺氧缺血后1,3,5,10 d各处死5只H IBD大鼠,免疫组化方法检测大鼠脑内GLUT1及GLUT3表达,并与对照组和假手术组比较。结果：正常新生大鼠脑内微血管即可见GLUT1表达。H IBD后1 d,缺血侧半球GLUT1表达略有增加,3 d达高峰,至5 d时仍高于正常,10 d基本恢复正常水平。H IBD后1 d,GLUT3表达无明显变化,3 d时GLUT3表达已明显减少,5 d时进一步减少,10 d时仍显著低于对照组。GLUT3表达减少最显著的部位为海马CA1区。结论：H IBD后脑内GLUT1和GLUT3的表达异常可导致脑能量代谢途径改变,加重缺氧缺血后神经元的损伤及影响损伤神经元的修复。

OBJECTIVE: In order to study the mechanisms of cerebral energy failure after hypoxic-ischemic brain damage (HIBD), the effects of hypoxia-ischemia (HI) on glucose transporter proteins (GLUT1 and GLUT3) expression in the brain were investigated in neonatal rats. METHODS: Thirty seven-day-old Wistar rats were randomly assigned into Normal (n=5), Sham-operated (n=5) and HIBD model groups (n=20). The HIBD model was established by ligating the right common carotid artery combined with the hypoxia exposure (8% oxygen). The rats were sacrificed at 1,3,5 and 10 days after HIBD. The expressions of GLUT1 and GLUT3 in the brain were examined by immunohistochemistry. RESULTS: Microvascular GLUT1 was seen in the Normal group. GLUT1 immunoreactivity began to increase in ipsilateral hemisphere 1 day after HI,peaked on the 3rd day, and remained high on the 5th day. No significant changes in GLUT3 immunoreactivity were observed 1 day after HI. Three days after HI, there was a pronounced decrease in GLUT3 staining; and on the 5th day the decrease of GLUT3 staining was most significantly. The maximal decrease of GLUT3 staining was seen in the hippocampal CA1 region. CONCLUSIONS: HI may result in an abnormal expression of glucose transporter proteins in the brain, which might aggravate the neuronal injury and interfere with its repair.