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Articles in PresS, published online ahead of print October 5, 2001
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00161.2001
Submitted on May 9, 2001
Accepted on September 26, 2001
1 Cardiovascular Research Institute, University of California San Francisco, San Francisco, CA, USA
* To whom correspondence should be addressed. E-mail: jkitter{at}itsa.ucsf.edu.
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 d gestation; fetuses were delivered at 21 or 22 d. 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 d, 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 airspace 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.
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