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The rearch for the factors that affect fetal lung maturation, and pathogenesis of fetal lung hypoplasia

影响胎肺成熟的因素及胎肺发育不全的发病机制研究

基本信息

批准号：
12671069
负责人：
IKEDA Kazushige
金额：
$ 2.05万
依托单位：
Keio University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2000
资助国家：
日本
起止时间：
2000 至 2002
项目状态：
已结题

项目摘要

BACKGROUNDThe prognosis of respiratory distress syndrome has been dramatically improved since synthetic surfactant was available. However, neonates with pulmonary hypoplasia have a high mortality despite advances in medical management, and the treatment of pulmonary hypoplasia remains difficult in neonatal medicine. The analysis of fetal lung structure during mid-gestation,especially around the threshold of viability, is important from the point of view of 1) the strategy to manage the babies with pulmonary hypoplasia, and 2) improvement of the prognosis of ultra-premature babies born less than 23 weeks gestation. We investigated the following subjects between April, 2000 and March, 2003:1.the basic research on treatment of lung hypoplasia following intrauterine exposure to nitrofen.2.lung maturation in a case of congenital tracheal agenesis.3.lung maturation of human fetuses in mid-gastation, especially 21 weeks gestation.4.threshold of viability from the point of view of birth weight.5.intrauterine expression of surfactant protein D in human fetuses.RESULTS1. Respiratory status of lung hypoplasia induced by nitrofen was improved by intratrachal administration of perflurocarbon.2. Lung maturation of fetal tracheal agenesis in mid-gestaion appeared to be more advanced than control group.3. The production of mature surfactant protein B in terminal airways is scarce at 21 weeks gestation, which is associated with the immature mechanism of proprotein processing in the cytoplasm.4. We reported an ultra-premature baby of 289 gram birth weight, who is born June 1999.5. The production of surfactant protein D in human fetal lungs begins in bronchiolar and terminal airways from about 21 weeks gestation.

背景自合成表面活性剂问世以来，呼吸窘迫综合征的预后已显著改善。然而，尽管医疗管理取得了进步，但新生儿肺发育不全的死亡率很高，肺发育不全的治疗仍然是新生儿医学的难点。分析妊娠中期，尤其是存活阈值前后胎儿肺结构，对于1)肺发育不全患儿的处理策略，2)改善妊娠小于23周的超早产儿的预后具有重要意义。我们于2000年4月至2003年3月调查了以下受试者：1。硝基芬宫内暴露后肺发育不全治疗的基础研究先天性气管发育迟缓1例肺成熟。人妊娠中期胎儿的肺成熟，特别是妊娠21周。5.表面活性剂蛋白D在人胎儿宫内的表达。经气管内灌注全氟碳化合物可改善硝芬所致肺发育不全的呼吸状态。妊娠中期胎儿气管发育不全的肺成熟时间明显早于对照组。妊娠21周末气道中成熟表面活性剂蛋白B的产生较少，这与细胞质中蛋白加工的不成熟机制有关。我们报告了一名出生体重289克的超早产儿，生于1999.5年6月。人胎儿肺表面活性剂蛋白D的产生始于妊娠21周左右的细支气管和终末气道。