Lilien L D, Rosenfield R L, Baccaro M M, Pildes R S
J Pediatr. 1979 Mar;94(3):454-9. doi: 10.1016/s0022-3476(79)80601-0.
The metabolic responses to a constant glucose infusion were measured in 30 premature infants, 700 to 1,550 gm. The study included 18 stressed premature infants who needed assisted ventilation, and 12 control premature infants. Metabolic measurements were similar in both groups in the cord and preinfusion samples. In the first postinfusion sample, glucose, cortisol, and glycerol values were higher in stressed than in control premature infants. Hyperglycemia was seen in 13 of stressed and in only one of control premature infants. Stressed infants who became hyperglycemic in the first postinfusion sample were then compared to stressed euglycemic infants. Insulin levels were higher, glycerol levels similar, but cortisol levels lower in stressed hyperglycemic than in stressed euglycemic premature infants. The etiology of hyperglycemia in stressed premature infants cannot be attributed to hypoinsulinemia or to hypercortisolemia, and is not associated with increased glycerol levels. There was no difference in mortality between stressed hyperglycemia and stressed euglycemic infants; stress, rather than hyperglycemia, was related to mortality.
对30名体重在700至1550克的早产儿进行了持续葡萄糖输注的代谢反应测量。该研究包括18名需要辅助通气的应激早产儿和12名对照早产儿。两组的脐带血和输注前样本的代谢测量结果相似。在输注后的第一个样本中，应激早产儿的葡萄糖、皮质醇和甘油值高于对照早产儿。13名应激早产儿出现高血糖，而对照早产儿中只有1名出现高血糖。然后将输注后第一个样本中出现高血糖的应激早产儿与血糖正常的应激早产儿进行比较。应激高血糖早产儿的胰岛素水平较高，甘油水平相似，但皮质醇水平低于应激血糖正常的早产儿。应激早产儿高血糖的病因不能归因于胰岛素缺乏或皮质醇过多，也与甘油水平升高无关。应激高血糖早产儿和应激血糖正常早产儿的死亡率没有差异；与死亡率相关的是应激，而非高血糖。
