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胎儿肺的成熟,与肺泡里层Ⅱ型细胞合成卵磷脂有关。这一过程的紊乱导致RDS。临床所见RDS不仅发生于早产儿,同样也出现在糖尿病母亲所生的足月婴儿。这一事实提示:母亲的糖尿病由于某种原因阻碍胎儿肺的成熟。作者测定妊娠20天的链脲霉素糖尿病鼠(血糖>25mmol/L)胎鼠及正常对照鼠肺的卵磷脂生物合成。而且测定了用胰岛素治疗糖尿病鼠的20日龄胎鼠的卵磷脂生物合成。显性糖尿病鼠的胎儿显示体重减低,胰腺的胰岛素储存明显减少。与对照相比,这些胎鼠卵磷脂的生物合成明显减低。胰岛
Fetal lung maturation, and type II cells in the alveolar layer of synthetic lecithin. The disorder of this process leads to RDS. Clinical findings RDS not only occurs in premature children, also appeared in full-term infants born to diabetic mothers. This fact suggests that: mother’s diabetes hinder fetal lung maturity for some reason. The authors determined the lecithin biosynthesis in the lungs of streptozotocin-diabetic (glucose> 25 mmol / L) fetuses and normal control mice at 20 days of gestation. Furthermore, the lecithin biosynthesis of 20-day-old fetuses treated with insulin for diabetic mice was measured. Fetal diabetes in dominant diabetic mice showed a decrease in body weight and a significant reduction in pancreatic insulin stores. The biosynthesis of these fetal rat lecithins was significantly reduced compared to the control. Islet