Vannucci R C, Vasta F, Vannucci S J
Pediatr Res. 1987 Jun;21(6):524-9. doi: 10.1203/00006450-198706000-00002.
Unlike adult rats, glucose supplementation of immature rats does not lead to accentuated hypoxic-ischemic brain damage. To explore the reason for this age-specific paradox, we subjected 7-day postnatal rats to unilateral common carotid artery occlusion followed by a subcutaneous injection of either 0.1 ml 50% glucose or normal saline. They were then exposed to hypoxia with 8% oxygen, during which they received 2.5 microCi 2-[14C]-glucose or were quick-frozen for brain metabolite analysis. During hypoxia-ischemia, glucose transport into the ipsilateral cerebral hemisphere of the hyperglycemic rats was greater (+100-150%) than in normoglycemic animals. However, glucose consumption was similar in the two groups. Glucose concentrations in brain were lower during hypoxia-ischemia in the normoglycemic animals, whereas lactate increased to similar levels in the two groups. The high-energy phosphate reserves, ATP and phosphocreatine, were depleted to a similar extent. Thus, hyperglycemia combined with hypoxia-ischemia, although associated with increased glucose transport into brain, does not lead to enhanced glucose utilization or lactate accumulation by brain over that of hypoxia-ischemia alone.
与成年大鼠不同，给未成熟大鼠补充葡萄糖不会导致更严重的缺氧缺血性脑损伤。为探究这种年龄特异性矛盾现象的原因，我们对出生后7天的大鼠进行单侧颈总动脉闭塞，随后皮下注射0.1 ml 50%葡萄糖或生理盐水。然后将它们置于含8%氧气的低氧环境中，在此期间，它们接受2.5微居里的2-[14C]-葡萄糖，或者被快速冷冻以进行脑代谢物分析。在缺氧缺血期间，高血糖大鼠同侧脑半球的葡萄糖转运比正常血糖动物更大（增加100 - 150%）。然而，两组的葡萄糖消耗相似。正常血糖动物在缺氧缺血期间脑内葡萄糖浓度较低，而两组的乳酸水平升高至相似程度。高能磷酸储备，即三磷酸腺苷（ATP）和磷酸肌酸，消耗程度相似。因此，高血糖与缺氧缺血相结合，尽管会使脑内葡萄糖转运增加，但不会导致脑内葡萄糖利用增强或乳酸积累超过单纯缺氧缺血时的水平。
