LUNG GAS-EXCHANGE SURFACE--FORMATION AND REGULATION

球囊变薄、分离和细胞组成的变化 组成了未成熟肺的气体交换区，而 隔后肺泡数和平均肺泡体积增加， 气体交换表面积(Sa)和气体交换面积(Sa)之间的关系 生物体代谢率(VO2)。我们的研究表明，或正在 与之一致，以下是新的信息和想法：1)意思是“他” 在分隔期形成的肺泡最多。 “分流”；2)在分流过程中不可撤销地塞米松(Dex)治疗 阻断间隔，减慢形成肺泡的“其他”方式的速度 即使在地塞米松治疗停止后；3)地塞米松诱导的影响包括 提前完成看似正常的相对变化 肺泡壁的细胞组成；4)临床上相关的短- 使用地塞米松的足月产前治疗对出生时的Sa没有影响，但 表现为出生后Sa增加减少；5)甲状腺激素，在 不增加VO2的剂量会加速Sa在出生后的增加。 我们将继续利用新的体视学方法：1) 检验短期(3天)地塞米松晚期治疗的假设 妊娠期或“分隔期”可能过早和 永久终止(或减少)隔膜或“其他”形成方式 而这种影响发生在正常牙槽提前完成的情况下 气体的绝对细胞组成的发展演变- 交换墙；2)确定甲状腺的构筑机制 激素，在非生热剂量，加速出生后早期增加 在Sa中，阐明其对气体交换的细胞组成的影响。 WALL(与地塞米松的效果对比)，并测试甲状腺激素 能克服牙槽骨形成的地塞米松障碍和Sa的增加； 3)“记号”已形成肺，以测试隔膜后是否有新的肺泡 形成主要发生在肺泡-胸膜交界处。我们认为我们的 先前的结果表明我们的方法是可行的，并且，强 我们可能会对一个被忽视但 肺发育在生理和临床上的重要方面。

Thinning, septation, and change in cellular composition of the saccules that compose the gas-exchange region of the immature lung, and the postseptation increase in alveolar number and average alveolar volume, effect the relation between the gas-exchange surface area (Sa) and the organism's metabolic rate (VO2). Our studies demonstrate, or are consistent with, the following new information and ideas: 1) means "other" than septation produce most alveoli formed during the period of "septation"; 2) dexamethasone (Dex) treatment during septation irrevocably blocks septation, and slows the rate of "other" means of forming alveoli even after Dex-treatment is stopped; 3) the Dex-induced effects include the premature completion of the seemingly normal changes in the relative cellular composition of the alveolar wall; 4) clinically relevant short- term prenatal treatment with Dex does not affect Sa at birth but is expressed as diminished postnatal increase in Sa; 5) thyroid hormone, in doses that do not increase VO2, accelerates the postnatal increase of Sa. We will continue to take advantage of new stereological methods to: 1) test the hypothesis that short-term (3 days) Dex treatment in late gestation or during the period of "septation" can prematurely and permanently terminate (or diminish) septation or "other" means of forming alveoli and that this effect occurs with premature completion of the normal developmental evolution of the absolute cellular composition of the gas- exchange wall; 2) determine the architectural mechanism by which thyroid hormone, in non-calorigenic doses, accelerates the early postnatal increase in Sa, elucidate its effect on the cellular composition of the gas-exchange wall (contrasting it with the effect of Dex), and, test if thyroid hormone can overcome the Dex-impairment of alveolus formation and increase of Sa; 3) "mark" already formed lung to test if, after septation, new alveolus formation occurs mainly at the alveolar-pleural interface. We think our prior results show the feasibility of our approach, and, the strong likelihood we will provide substantial new insights into a neglected but physiologically and clinically important aspect of lung development.