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健康新生儿及患有透明膜病的婴儿体内前列腺素E和F2α的尿排泄情况。

Urinary excretion of prostaglandin E and F 2 alpha in healthy newborn infants and in infants with hyaline membrane disease.

作者信息

Csaba I F, Sulyok E, Ertl T

出版信息

Acta Paediatr Acad Sci Hung. 1979;20(2-3):193-8.

PMID:546017
Abstract

Urinary PGE and PGF 2 alpha excretion was estimated in 11 healthy full-term (mean birth weight, 3327 g; mean gestational age, 39.2 weeks). 15 healthy preterm (mean birth weight, 1722 g; mean gestational age, 32.1 weeks) and in 9 preterm infants suffering from hyaline membrane disease (HMD) (mean birth weight: 1454 g, mean gestational age: 31 weeks). Measurements were carried out on the 1st, 3rd and 5th days of life by radioimmunoassay, using Clinical Assays Inc. RIA kits. Urinary PGE excretion on the first day of life was 3.76 +/- 0.41 ng/day, 2.43 +/- 0.65 ng/day and 1.19 +/- 0.27 ng/day for healthy full-term, healthy premature and premature infants with HMD, respectively. The differences were significant at the level of p less than 0.05. With advancing postnatal age urinary PGE excretion markedly increased in each group (p less than 0.05). Urinary PGF 2 alpha excretion on the first day was 10.8 +/- 2.0 ng/day in full-term, 6.6 +/- 2.2 ng/day in healthy premature and 4.35 +/- 1.9 ng/day in premature infants with HMD. Then an inconsistent rise could be observed without statistically significant difference between the individual groups of various postnatal age and between the different groups of the same postnatal age. The decreased renal PGE production is suggested to be involved in the pathomechanism of HMD.

摘要

对11名健康足月儿(平均出生体重3327克;平均胎龄39.2周)、15名健康早产儿(平均出生体重1722克;平均胎龄32.1周)以及9名患有透明膜病(HMD)的早产儿(平均出生体重1454克;平均胎龄31周)的尿中前列腺素E(PGE)和前列腺素F2α(PGF2α)排泄量进行了评估。在出生后的第1、3和5天,使用Clinical Assays Inc.的放射免疫分析试剂盒通过放射免疫法进行测量。健康足月儿、健康早产儿和患有HMD的早产儿出生第一天的尿PGE排泄量分别为3.76±0.41纳克/天、2.43±0.65纳克/天和1.19±0.27纳克/天。差异在p<0.05水平具有统计学意义。随着出生后年龄的增加,每组尿PGE排泄量均显著增加(p<0.05)。足月新生儿出生第一天的尿PGF2α排泄量为10.8±2.0纳克/天,健康早产儿为6.6±2.2纳克/天,患有HMD的早产儿为4.35±1.9纳克/天。随后可观察到一种不一致的上升,在不同出生后年龄的各个组之间以及相同出生后年龄的不同组之间无统计学显著差异。肾PGE生成减少被认为与HMD的发病机制有关。

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