中文摘要：

目的探讨血糖对缺氧缺血（HI）新生大鼠脑内葡萄糖转运蛋白I（GLUT1）基因表达的影响。方法对7日龄sD新生大鼠通过调节25％葡萄糖的注射次数、时间或禁食12h，分别建立单纯低血糖组、HI组、HI前低血糖组、HI后低血糖组、HI前轻度高血糖组、HI后轻度高血糖组、HI前重度高血糖组以及HI后重度高血糖组；另设正常组和假手术组。应用逆转录PCR（RT—PCR）方法，分别在HI后2、24、48、72h及7d对各组新生大鼠脑内GLUT1基因进行测定。结果正常组GLUT1基因表达量随日龄增加而增高。HI可引起GLUT1基因表达量的短期上调，至HI后72h及7d则非常显著地低于正常组（P〈0．01）。HI前低血糖组GLUT1基因在HI后各时段均低于曾经HT各组，其中HI后48h及HI后7d显著低于HI组（P均〈0．05）。HI前重度高血糖可明显上调GLUT1基因表达量，在HI后多数时段的表达量均显著高于曾经HI各组（P〈0．05或0．01）。HI前轻度高血糖对GLUT1基因表达的影响不如HI前重度高血糖组。在Ⅲ后无论轻或重度高血糖组以及HI后低血糖组，其GLUT1基因表达时相均与H1前低血糖组类似。结论结合过去系列研究结果提示，HI前低血糖可使GLUT1基因表达和产物合成明显下调、脑病理改变加重；HI前重度高血糖则使GLUTI基因表达和产物合成明显上调、脑病理改变显著改善。提示在HI前预先补充足量葡萄糖，有可能在一定程度上提高脑内应对HI的侵袭、改善缺氧缺血程度的能力。

英文摘要：

Objective To explore the effect of different blood glucose levels on the expression of cerebral GLUT1 mRNA in neonatal rats with hypoxic ischemia （HI）. Methods Seven-day-old neonatal SD rats were randomly divided into 10 groups consisting of normal group, sham group, group with hypoglycemia, HI group, group with hypoglycemia before HI, group with hypoglycemia after HI, group with mild hyperglycemia before HI, group with mild hyperglycemia after HI, group with higher hyperglycemia before HI, and group with higher hyperglycemia after HI. The expression of GLUT1 mRNA was detected with RT-PCR technique in all neonatal rats of 10 groups at 2,24,48,72 h and 7d after HI. Results There was an enhancement in the expression of GLUT1 mRNA with increase of day age in normal control groups. HI could significantly enhance the expression of GLUT1 mRNA in the short period after HI with a peak at 24 h after HI, and then significantly lower than those in control group at 72 h and 7 d after HI （allP 〈0. 01 ）. The expression of GLUT1 mRNA in the group with hypoglycemia before HI was lower than those in the all groups with HI in each time interval after HI, in particular at 48 h and 7 d after HI （ all P 〈 O. 05 ）. The expression of GLUT1 mRNA could be up-regulated by higher hyperglycemia before HI,and the expressional levels of GLUT1 mRNA in the group with higher hyperglycemia before HI were higher than those in all groups with HI in the most time intervals after HI （ P 〈0. 05 or 0. 01 ）. There was no significant influence of mild hyperglycemia before HI on the expression of GLUTI mRNA. The similar expressional time phase of GLUT1 mRNA was observed in either groups with mild or higher hyperglycemia after HI or group with hypoglycemia after HI comparing to that in group with hypoglycemia before HI. Conclusion Related to serial results published before, it is concluded that the expression of GLUT1 mRNA and the synthesis of GLUT1 can be down-regulated by hypoglycemia with aggravation of crebral pathology, and up-r