Stimulation of lung growth by tracheal obstruction in fetal sheep: Relation to luminal pressure and lung liquid volume
Stimulation of lung growth by tracheal obstruction in fetal sheep: Relation to luminal pressure and lung liquid volume
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DOI：
10.1203/00006450-199802000-00005
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发表时间：
1998-02-01
影响因子：
3.6
通讯作者：
Harding, R
中科院分区：
文献类型：
--
作者：
Nardo, L;Hooper, SB;Harding, R
胎儿气管阻塞导致液体在未来的气道内积聚，这是肺生长的有力刺激。我们的目的是确定气管阻塞后胎肺生长的增加与肺液体量和气管压力增加之间的关系，以更好地了解生长反应的机制。测定气管阻塞4和10 d对肺DNA和蛋白质含量以及DNA合成率的影响;这些数据与气管阻塞2和7 d后收集的数据相结合。胎肺液体体积和分泌率进行了测量前（D 0）和第1，2，4，7和10天后，气管阻塞;胎气管压力进行了监测，在整个期间。在气管阻塞的1天内，气管压力从2.9 +/- 0.8 mm Hg（对照）增加到4.3 +/- 0.4 mm Hg，并在阻塞期间保持在该升高水平。肺液体量从第0天的24.7 +/- 1.1 mL/kg逐渐增加至气管阻塞第7天的97.3 +/- 15.2 mL/kg，但到第10天没有进一步增加。气管阻塞显着增加肺DNA和蛋白质含量高于对照值，在10天期间，肺DNA含量的增加密切相关（r = 0.99），肺液体体积的增加，但不增加气管压力。DNA合成率增加4天的气管阻塞（66%），但已恢复到控制水平的第10天。我们的结论是：1）负责由气管阻塞诱导的肺生长加速的机制在第2天最活跃，在第4和第7天以降低的水平保持活跃，并且在第10天恢复到对照水平;和2）气管阻塞期间（第2-7天）肺DNA含量的增加与肺液体体积的增加密切相关，但与管腔内压力的增加无关。因此，我们认为肺扩张的增加是气管阻塞引起胎肺生长加速的主要因素之一。
Obstruction of the fetal trachea causes liquid to accumulate within the future airways, which is a potent stimulus for lung growth. Our aim was to determine the relationship between the increase in fetal lung growth after tracheal obstruction and the increases in lung liquid volume and tracheal pressure to better understand the mechanisms involved in the growth response. The effects of 4 and 10 d of tracheal obstruction on lung DNA and protein contents and DNA synthesis rates were determined; these data were combined with data collected previously after 2 and 7 d of tracheal obstruction. Fetal lung liquid volumes and secretion rates were measured before (d 0) and on d 1, 2, 4, 7, and 10 after tracheal obstruction; fetal tracheal pressures were monitored throughout this period. Tracheal pressures increased from 2.9 +/- 0.8 mm Hg (control) to 4.3 +/- 0.4 mm Hg within 1 d of tracheal obstruction and remained at this elevated level for the duration of the obstruction period. Lung liquid volume increased progressively from 24.7 +/- 1.1 mL/kg on d 0 to 97.3 +/- 15.2 mL/kg at d 7 of tracheal obstruction, but had not increased further by d 10. Tracheal obstruction significantly increased lung DNA and protein contents above control values; over the 10-d period the increase in lung DNA content was closely related (r = 0.99) to the increase in lung liquid volume, but not to the increase in tracheal pressure. DNA synthesis rates were increased at 4 d of tracheal obstruction (by 66%) but had returned to control levels by d 10. We conclude that: 1) the mechanisms responsible for the acceleration in lung growth induced by tracheal obstruction are most active on d 2, remain active at a reduced level on d 4 and 7, and have returned to control levels by d 10; and 2) the increase in lung DNA content during tracheal obstruction (d 2-7) is closely related to the increase in lung liquid volume, but not to the increase in intraluminal pressure. Thus, we suggest that an increase in lung expansion is one of the primary factors responsible for the acceleration in fetal lung growth induced by tracheal obstruction.