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影响新生儿表面活性剂成分的因素。

Factors influencing surfactant composition in the newborn infant.

作者信息

Obladen M

出版信息

Eur J Pediatr. 1978 Jul 3;128(3):129-43. doi: 10.1007/BF00444298.

Abstract

In order to evaluate the surfactant maturation of the neonate, tracheal aspirates were analyzed in 84 newborn infants with 12h of birth. Using 2-dimensional thin-layer chromatography, 9 different phospholipids were identified. Dynamic surface tension measurements were performed with a modified Wilhelmy balance. Five different groups of infants with typical phospholipid patterns were characterized: i.e., 1. Normal term newborn. 2. RDS in the preterm infant. 3. Acceleration of lung maturity in preterm infants without RDS. 4. Retardation in term infants with RDS. 5. Therapeutic induction of pulmonary maturity in preterm infants following maternal glucocorticoid administration. Mature lung effluent contains high concentrations of phosphatidylcholine (PC) and phsophatidylglycerol (PG). In infants with RDS, PC is low and PG absent. Accelerated lung maturity was observed after chronic prenatal stress, such as prolonged rupture of the membranes, chronic vaginal bleeding, and maternal hepatitis or drug addiction. Retardation of pulmonary maturity was seen in infants with alpha-1-AT-deficiency, maternal diabetes and maternal hypothyroidism. Administration of methylprednisolone to the mother 24 h to 72h before birth induced both the synthesis of PC and PG in the preterm infants, resulting in an almost full-term phospholipid pattern as early as 31 weeks of gestation. The significance of these factors on the pathogenesis of RDS is discussed.

摘要

为评估新生儿的表面活性剂成熟度,对84例出生12小时内的新生儿的气管吸出物进行了分析。采用二维薄层色谱法鉴定出9种不同的磷脂。使用改良的威尔海姆天平进行动态表面张力测量。确定了具有典型磷脂模式的五组不同婴儿:即1. 足月正常新生儿。2. 早产儿呼吸窘迫综合征。3. 无呼吸窘迫综合征的早产儿肺成熟加速。4. 足月呼吸窘迫综合征婴儿肺成熟延迟。5. 母体给予糖皮质激素后早产儿肺成熟的治疗性诱导。成熟肺流出物含有高浓度的磷脂酰胆碱(PC)和磷脂酰甘油(PG)。患有呼吸窘迫综合征的婴儿中,PC含量低且无PG。在慢性产前应激后观察到肺成熟加速,如胎膜早破、慢性阴道出血、母体肝炎或药物成瘾。在α-1-抗胰蛋白酶缺乏、母体糖尿病和母体甲状腺功能减退的婴儿中可见肺成熟延迟。在出生前24至72小时给母体注射甲基强的松龙可诱导早产儿合成PC和PG,早在妊娠31周时就产生几乎足月的磷脂模式。讨论了这些因素对呼吸窘迫综合征发病机制的意义。

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