Main pulmonary artery ligation reduces lung fluid production in fetal sheep.

Pulmonary hypoplasia is increasing as a cause of neonatal death. To understand the pathophysiology of pulmonary hypoplasia, the physiology of fetal lung growth must first be understood. Lung fluid production and fetal breathing are primary factors regulating lung growth. Interruption of pulmonary arterial flow also decreases fetal lung growth. To define the relationship of pulmonary arterial flow to other factors known to be important for fetal lung growth, breathing and lung fluid production were measured after postductal main pulmonary artery (MPA) ligation in fetal sheep. Surgical preparation at 107-116 d gestation included placement of vascular catheters and a tracheal catheter connected to an intrauterine collection bag for lung fluid. Five fetuses served as monitored controls (catheters only), 3 as sham operated controls (catheters and thoracotomy), and 7 had MPA ligation. MPA ligation significantly decreased lung weights at 131-140 d; mean dry weight (g): MPA ligation--6.7, sham--23.4, monitored--22.3. Mean rates of lung fluid production (mL/h) were also decreased (d gestation): 116-122 d: MPA ligation--2.2, sham--9.1, monitored--6.8; 123-129 d: MPA ligation--2.1, sham--9.1, monitored--6.2; 130-136 d: MPA ligation--1.5, sham--12.4, monitored--7.7. There were no differences between MPA ligated, sham, and monitored fetuses in the incidence or intensity of fetal breathing movements. Decreased lung fluid production after main pulmonary artery ligation is most likely due to decreased secretion of lung fluid. Pulmonary arterial flow in other models of pulmonary hypoplasia which decrease lung fluid production (i.e., oligohydramnios) should also be examined.