Experimental pulmonary hypoplasia due to oligohydramnios and its reversal by relieving thoracic compression.

To investigate the role of thoracic compression in the etiology of pulmonary hypoplasia associated with oligohydramnios, we shunted amniotic fluid into the maternal abdominal cavity at 25-days gestation in one group of fetal rabbits and occluded the bladder outlet in another. Bladder-neck obstruction produced severe bilateral hydronephrosis. Both procedures produced oligohydramnios (amniotic fluid volume reduced, p less than .001) at reexploration on day 28. At term (day 31) newborns undergoing these procedures had significantly decreased lung weights (p less than .01). Lung histology was not affected. To determine whether decompression of the thorax would prevent pulmonary hypoplasia, another group of fetuses had their bladders occluded and underwent one of two procedures to relieve thoracic compression. In one group, amniotic fluid volume was restored by a constant infusion of normal saline. In the other, opening the abdomen and allowing viscera to herniate avoided thoracic compression from a diaphragm elevated by a dilated urinary tract and ascites. Liveborn obstructed rabbits undergoing either procedure had increased lung weight-to-body weight ratios compared to those in newborns undergoing only the obstructive procedure (p less than 0.05). These experiments suggest that mechanical restriction to lung growth plays a role in the development of pulmonary hypoplasia associated with oligohydramnios, and that pulmonary hypoplasia may be partially reversible by procedures which reduce thoracic compression.