GLUCOSE TURNOVER IN INFANTS WITH CEREBRAL INJURY

需要新技术来识别处于危险中的危重婴儿 神经系统发育异常 该项目将决定 如果通过稳定的葡萄糖产生速率（GPR）测量 同位素技术可以提高脑损伤的评估， 新生儿 这种方法的基础是发展 用于研究CNS代谢功能的简化技术是 估计的脑重量和整体之间的线性相关性， 早产儿至成人的血糖转换率（r=0.94）。 初步研究还表明， 皮质脑块的GPR较低。我们对GPR的初步研究， 危重新生儿表明，10/11的婴儿，与GPR 低于按体重预测的预期值的50%，死亡或 没有超过胎儿期的神经系统发育。 中 合同，6名危重但神经正常的婴儿的GPR， 研究了两个或两个以上的场合，变化的平均只有18%， 在新生儿重症监护室的过程中。 这些 数据表明，低GPR的发现可以补充现有的 技术在早期识别婴儿神经系统疾病中的应用 损害 我们建议测试的假设，低GPR是一个 早期预测新生儿死亡或严重脑损伤。 评估 作为临床试验的灵敏度和特异性， 必须建立GPR的正常范围。 我们将 通过确定GPR确定范围， 100名神经系统结果正常的危重婴儿。 为了实现这些目标，我们将进行气相色谱分析- 对获得的6份0.3cc血清样本进行质谱分析 在床边，四小时的输液过程中， 二氘代葡萄糖这些研究将测试 低GPR和神经学结果。 建立低GPR 作为异常脑细胞代谢活动的早期预测因子， 有助于识别神经系统受损的婴儿， 协助评估新的治疗方法， 脑损伤的治疗。

New technologies are needed to identify critically-ill infants at risk for abnormal neurological development. This project will determine if the measurement of the glucose production rate (GPR) by stable isotope technology can enhance the assessment of brain damage in newborn infants. The basis of this approach to the development of simplified techniques for the study of CNS metabolic function is the linear correlation between estimated brain weight and whole- body glucose turnover found in premature infants to adults (r=0.94). Preliminary studies have also shown that infants with extensive loss of cortical brain mass have low GPR. Our pilot study of GPRs in critically-ill newborns demonstrated that 10/11 infants, with a GPR of less than 50% of the expected value predicted by weight, died or did not progress past fetal stages of neurological development. In a contract, GPRs of six critically ill, but neurologically normal infants, studied on two or more occasions, varied an average of only 18% over the course of the infant in neonatal intensive care unit. These data suggest that the finding of a low GPR may complement existing technology in the early identification of infants with neurologic damage. We propose to test the hypothesis that a low GPR is an early predictor of neonatal death or severe brain injury. To assess the sensitivity and specificity of the GPR as a clinical test, it is also necessary to establish the normal range of the GPR. We will establish a range by determination of the GPR in a minimum of 100 critically ill infants whose neurological outcomes are normal. To accomplish these aims, we will perform gas chromatography- mass spectrometry analysis of six 0.3cc serum samples obtained from the infants during a bedside, four-hour infusion of dideuteroglucose. These studies will test the correlations between low GPR and neurological outcome. Establishment of a low GPR as an early predictor of abnormal brain cell metabolic activity will facilitate the identification of neurologically damaged infants and assist in the evaluation of new therapeutic modalities for the treatment of brain injury.