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从人羊水中分离出的板层小体组分的发育研究。

Developmental study of a lamellar body fraction isolated from human amniotic fluid.

作者信息

Oulton M, Martin T R, Faulkner G T, Stinson D, Johnson J P

出版信息

Pediatr Res. 1980 May;14(5):722-8. doi: 10.1203/00006450-198005000-00004.

DOI:10.1203/00006450-198005000-00004
PMID:6892955
Abstract

Several properties of a pellet fraction obtained on centrifuging amniotic fluid at 10,000 X g for 20 min were investigated. From these analyses, we defined a developmental profile which appears to describe the maturational process of the fetal lung surfactant system. At 14 to 18 wk gestation, the pellet fraction consisted of membrane-bound vesicles without internal lamellae. The phospholipid composition did not resemble that of surfactant, the major phospholipid being sphingomyelin. This stage, designated as presurfactant, persisted until 30 to 32 wk gestation. After this time, the phospholipid concentration of the pellet fraction increased continuously throughout development, and gradual but continuous changes in phospholipid composition were observed. Lecithin and phosphatidylinositol increased between 30 and 35 wk gestation. Interruption of pregnancies at this stage, termed onset of surfactant synthesis, resulted in 100% incidence of respiratory distress syndrome. From 36 wk gestation to postterm, the pellet fraction contained structures with the characteristic morphology of the lamellar inclusion bodies. The presence of single membrane components in these preparations did not contribute to the phospholipid composition. Early formed lamellar bodies lacked phosphatidylglycerol and had a high content of phosphatidylinositol. Once phosphatidylglycerol appeared in the lamellar body fraction, it continued to increase, accompanied by a decrease in phosphatidylinositol with little change in lecithin. A phosphatidylglycerol value of greater than 1% of the total phospholipids appeared to represent the stage of maturity at which there was no risk of respiratory distress syndrome.

摘要

对羊水在10,000×g离心20分钟后获得的沉淀部分的几种特性进行了研究。通过这些分析,我们定义了一种发育概况,它似乎描述了胎儿肺表面活性剂系统的成熟过程。在妊娠14至18周时,沉淀部分由没有内部板层的膜结合囊泡组成。磷脂组成与表面活性剂不同,主要磷脂是鞘磷脂。这个阶段被称为前表面活性剂阶段,一直持续到妊娠30至32周。此后,沉淀部分的磷脂浓度在整个发育过程中持续增加,并且观察到磷脂组成逐渐但持续的变化。卵磷脂和磷脂酰肌醇在妊娠30至35周之间增加。在此阶段中断妊娠,即表面活性剂合成开始时,呼吸窘迫综合征的发生率为100%。从妊娠36周到期末,沉淀部分包含具有板层包涵体特征形态的结构。这些制剂中单个膜成分的存在对磷脂组成没有贡献。早期形成的板层小体缺乏磷脂酰甘油,磷脂酰肌醇含量高。一旦磷脂酰甘油出现在板层小体部分,它就会持续增加,同时磷脂酰肌醇减少,卵磷脂变化不大。磷脂酰甘油值大于总磷脂的1%似乎代表了没有呼吸窘迫综合征风险的成熟阶段。

相似文献

1
Developmental study of a lamellar body fraction isolated from human amniotic fluid.从人羊水中分离出的板层小体组分的发育研究。
Pediatr Res. 1980 May;14(5):722-8. doi: 10.1203/00006450-198005000-00004.
2
Amniotic fluid phospholipid profile as a predictor of fetal maturity in diabetic pregnancies.羊水磷脂谱作为糖尿病妊娠中胎儿成熟度的预测指标
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Respiratory distress syndrome, fetal pulmonary surfactant, and amniotic fluid phospholipid analysis.呼吸窘迫综合征、胎儿肺表面活性物质及羊水磷脂分析
Clin Lab Med. 1981 Jun;1(2):199-213.
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Comparison of lecithin: sphingomyelin ratio, fluorescence polarization, and phosphatidylglycerol in the amniotic fluid in the prediction of respiratory distress syndrome.羊水卵磷脂:鞘磷脂比值、荧光偏振及磷脂酰甘油在预测呼吸窘迫综合征中的比较
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Lung profile: sex differences in normal pregnancy.
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The effect of clinical characteristics on the lecithin/sphingomyelin ratio and lamellar body count: a cross-sectional study.临床特征对卵磷脂/鞘磷脂比值和板层小体计数的影响:一项横断面研究。
J Matern Fetal Neonatal Med. 2003 Dec;14(6):373-82. doi: 10.1080/14767050412331312210.
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Lamellar body phospholipid content of amniotic fluid and L/S ratio compared in assessing fetal lung maturity.
Clin Chem. 1980 May;26(6):766-9.
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Role of lamellar body count for the prediction of neonatal respiratory distress syndrome in non-diabetic pregnant women.板层小体计数在预测非糖尿病孕妇新生儿呼吸窘迫综合征中的作用。
Arch Gynecol Obstet. 2005 Apr;271(4):325-8. doi: 10.1007/s00404-004-0653-7. Epub 2004 Jun 18.
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Prevention of respiratory distress syndrome: Current view of fetal lung maturity studies.呼吸窘迫综合征的预防:胎儿肺成熟度研究的当前观点
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Relation of amniotic fluid lecithin/sphingomyelin ratio and fetal asphyxia to respiratory distress syndrome in premature infants.羊水卵磷脂/鞘磷脂比值及胎儿窒息与早产儿呼吸窘迫综合征的关系。
Can Med Assoc J. 1978 Jun 10;118(11):1384-9.

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