Experimental pulmonary hypoplasia and oligohydramnios: relative contributions of lung fluid and fetal breathing movements

Abstract

Inhibition of fetal breathing movements or increased loss of fetal lung fluid into the amniotic space have been suggested as two possible mechanisms causing pulmonary hypoplasia in the setting of oligohydramnios (OH). We examined the effect of OH produced by amniotic fluid shunting (AS) into the maternal abdominal cavity, ablation of fetal breathing by high cervical cord transection (CT), and CT and AS combined on fetal rabbit lungs at 24 days gestation. Lung growth at term (31 days) was measured by lung DNA content and wet lung weight. Compared to unoperated controls, newborns undergoing either AS alone or CT alone had much smaller lungs. When compared to CT alone, CT with AS resulted in a further significant decrease in lung growth. Thus, even when fetal breathing was eliminated by CT, AS caused further hypoplasia. If pulmonary hypoplasia in OH is related to increased loss of lung fluid, then tracheal ligation (TL) should prevent this process. TL combined with AS produced lungs with the same DNA content as controls, and thus the hypoplastic effects of OH were reversed by TL. Although fetal breathing is clearly important for lung growth, it appears that inhibition of fetal breathing is not the predominant etiology of oligohydramnios-related pulmonary hypoplasia. Fetal intrapulmonary fluid is formed by active transport across pulmonary epithelium, and may serve to distend potential airways and stimulate growth. These experiments suggest that lung hypoplasia associated with OH is related to loss of this internal stenting force.