Pre- and postnatal lung development, maturation, and plasticity - Effects of oligohydramnios on lung growth and maturation in the fetal rat

被引:33
作者
Kitterman, JA
Chapin, CJ
Vanderbilt, JN
Porta, NFM
Scavo, LM
Dobbs, LG
Ertsey, R
Goerke, J
机构
[1] Univ Calif San Francisco, Dept Pediat, San Francisco, CA 94143 USA
[2] Univ Calif San Francisco, Cardiovasc Res Inst, San Francisco, CA 94143 USA
[3] Univ Calif San Francisco, Dept Med, San Francisco, CA 94143 USA
[4] Univ Calif San Francisco, Dept Physiol, San Francisco, CA 94143 USA
关键词
fetal lung development; lung distension; pulmonary epithelial differentiation; pulmonary hypoplasia; pulmonary surfactant;
D O I
10.1152/ajplung.00161.2001
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Oligohydramnios (OH) retards fetal lung growth by producing less lung distension than normal. To examine effects of decreased distension on fetal lung development, we produced OH in rats by puncture of uterus and fetal membranes at 16 days of gestation; fetuses were delivered at 21 or 22 days of gestation. Controls were position-matched littermates in the opposite uterine horn. OH lungs had lower weights and less DNA, protein, and water, but no differences in saturated phosphatidylcholine, surfactant proteins (SP)-A and -B, and mRNA for SP-A, -B, -C, and -D. To evaluate effects on epithelial differentiation, we used RTI40 and RTII70, proteins specific in lung to luminal surfaces of alveolar type I and II cells, respectively. At 22 days of gestation, OH lungs had less RTI40 mRNA (P < 0.05) and protein (P < 0.001), but RTII70 did not differ from controls. With OH, type I cells (in proportion to type II cells) covered less distal air space perimeter (P < 0.01). We conclude that OH, which retards lung growth, has little effect on surfactant and impedes formation of type I cells relative to type II cells.
引用
收藏
页码:L431 / L439
页数:9
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