缺血缺氧性脑损伤(HIBD)的发生与脑组织能量耗竭、神经元结构和功能障碍有关。既往的研究显示，地塞米松预处理可产生脑保护作用。但关于缺氧缺血后，给予地塞米松及葡萄糖治疗对脑能量代谢影响的研究不多。本研究通过测定血糖、脑组织ATP生成率及ATP酶分解活性，了解地塞米松及葡萄糖治疗对缺氧缺血新生大鼠能量代谢的影响。

将7 d龄SD大鼠60只随机分成缺血缺氧性脑损伤组(HIBD组)、地塞米松治疗组及葡萄糖治疗组。3组动物经缺氧缺血处理后，HIBD组不做治疗、地塞米松组及葡萄糖治疗组分别以地塞米松及葡萄糖进行治疗。检测0 h，24 h，48 h，72 h实验大鼠的血糖、脑线粒体ATP生成率及ATP酶分解活性变化。

①缺氧缺血处理后，大鼠血糖、脑组织线粒体ATP生成率及ATP酶分解活性下降；②地塞米松治疗组ATP生成率24 h、48 h时较HIBD组高；ATP酶分解活性24 h时较HIBD组高；③葡萄糖治疗组脑组织线粒体ATP生成率48 h时较HIBD组高；④72 h时3组动物ATP生成率及ATP酶分解活性差异无显著意义；⑤地塞米松治疗组及葡萄糖治疗组的血糖在24 h时较HIBD组高；⑥48 h及72 h时，3组血糖值差异无显著意义。

地塞米松及葡萄糖可在短期内改善缺血缺氧新生大鼠脑组织能量供应，并对血糖产生影响。

To study the changes in blood sugar, mitochondrial ATP production rate and ATP synthase activity in dexamethasone treated and in glucose treated neonatal rats after hypoxic-ischemic brain damage.

7 days old rats were randomly assigned to HIBD group, dexamethasone treated group and glucose treated group. Had been made cerebral hypoxic-ischemic, the HIBD animals were divided into 0 h, 24 h, 48 h and 72 h groups; the dexamethasone treated animals and glucose treated animals were divided into 24 h, 48 h and 72 h groups and treated with dexamethasone and glucose separately. Then we examined changes in blood sugar, mitochondrial ATP production rate and ATP synthase activity.

① After hypoxic-ischemic, the rats' blood sugar, mitochondrial ATP production rate and ATP synthase activity were decreased. ②In dexamethasone treated group the ATP production rate at 24 h and 48 h, ATP synthase activity at 24 h were higher than HIBD group.③ In glucose treated group, the ATP production rate at 48 h were higher than HIBD group.④ At 72 h, there were no differences in mitochondrial ATP production rate and ATP synthase activity between 3 groups.⑤ The blood sugar in dexamethasone treated group and in glucose treated group were higher than HIBD group at 24 h.⑥ At 48 h and 72 h, there were no differences in blood sugar between 3 groups.

Dexamethasone and glucose improved HIBD rats' cerebral energy metabolize in a short term and affected blood glucose.