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Am J Physiol Lung Cell Mol Physiol 282: L431-L439, 2002. First published October 5, 2001; doi:10.1152/ajplung.00161.2001
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Vol. 282, Issue 3, L431-L439, March 2002

SPECIAL TOPIC
Pre- and Postnatal Lung Development, Maturation, and Plasticity
Effects of oligohydramnios on lung growth and maturation in the fetal rat

Joseph A. Kitterman, Cheryl J. Chapin, Jeff N. Vanderbilt, Nicolas F. M. Porta, Louis M. Scavo, Leland G. Dobbs, Robert Ertsey, and Jon Goerke

Cardiovascular Research Institute and Departments of Pediatrics, Medicine, and Physiology, University of California, San Francisco, California 94143

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.

fetal lung development; lung distension; pulmonary epithelial differentiation; pulmonary hypoplasia; pulmonary surfactant


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