Abstract
Arterio-venous extracorporeal membrane oxygenation (A-V ECMO) was established in goat fetuses via the umbilical vessels following incubation in a warm bath. The effect of A-V ECMO on fetal lung growth and maturation was evaluated. Eight goat fetuses of 120-130 days' gestation (trem, 150 days) were subjected to this immersion ECMO system. Tracheal ligation was performed on four fetuses (tracheal occlusion group). Tracheal ligation was not performed on the other four fetuses (trachea-open group). Four littermate fetuses with similar body weights were harvested and examined as baseline data before ECMO was performed (non-ECMO group). The mean duration of A-V ECMO was 107±41 h in the trachea-open group, and 139±67 h in the tracheal occlusion group. Mean fetal weight after ECMO was significantly higher than at the time of initiation of ECMO in the tracheal occlusion group. Phosphatidylcholine and disaturated phosphatidyl-choline in the lung tissue after ECMO were significantly higher in the tracheal occlusion group than in the non-ECMO group. Wet lung weight after ECMO was significantly higher in the tracheal occlusion group than in the non-ECMO group. Dry lung weight and dry lung weight/body weight were significantly higher in the tracheal occlusin group than in the non-ECMO group. Electron microscopy demonstrated a higher increase in type II cells/alveolar epithelial cells in the tracheal occlusion and trachea-open groups than in the non-ECMO group. Plasma cortisol levels were significantly higher in the tracheal occlusion group than in the non-ECMO group. T3 levels were significantly higher in the tracheal occlusion group as compared with the trachea-open group, and significantly higher in the trachea-open group as compared with the non-ECMO group. Fetal breathing movement appeared in two fetuses in the trachea-open group and two fetuses in the tracheal occlusion group. In this immersion fetal A-V ECMO system, tracheal occlusion affected the production of surfactant, and caused an increase in lung weight and type II alveolar epithelial cells.