Antepartum administration of aminophylline to pregnant rabbits resulted in accelerated formation of phospholipids regarded to be important components of pulmonary surfactant. Increases in the tissue content and synthesis of saturated phosphatidylcholine and phosphatidylinositol were found in lung slice preparations obtained from fetuses previously treated with aminophylline. Synthesis of phospholipids was measured using labeled palmitate, oleate, and glucose as precursors. The results showed increased de novo production of these lipids, and that glucose and glycogen may serve as important precursors. There was a significant reduction in triglyceride content while free fatty acids increased suggesting increased lipolysis in the aminophylline-treated groups, but this did not measurably affect the rate of labeled palmitate incorporation into total phospholipids.

Summary: Rabbits delivered at 27.0 days of gestation were studied after administration of cortisol (2 mg/kg/day), aminophylline (6.25 mg/kg/day), or sterile saline to the does on days 24–26 of gestation. Survival at 60 min was 52.9% in the aminophylline-treated group and 22.2% in the control and cortisol-treated groups with all animals being in a warm, oxygen-enriched environment and receiving frequent tactile stimulation. Lung volume at 30 cm H2O was lower in the cortisol-treated group than in the controls or aminophylline-treated group in animals surviving for 60 min (Table 2). The aminophylline-treated group retained significantly more gas at low pressures on the deflation curve (Table 2) and had significantly more phosphati-dylcholine recovered in lung lavage fluid (Table 3) than the other groups. Aminophylline appears to have enhanced lung maturation better than cortisol in this experimental model. Speculation: Improved survival of prematurely delivered rabbits after aminophylline administration (as compared with cortisol) may be due to a combination of factors including enhanced maturation of the lungs as well as stimulation of the respiratory center.

5% dextrose (D), 10%D, or 20%D with casein hydrolysate was administered at 120 ml/Kg/day, with an infusion pump, to 30, 1Kg rabbits via polyvinyl catheters placed into the aorta via a femoral artery. The catheter tip was located just above either the superior mesenteric artery(H) or the bifurcation(L). After 1-15 days the animals were sacrificed and examined. Complications found were aortic thrombosis or renal, hepatic, splenic, or GI infarction. 20 animals had catheters for ≥6 days(1g): all 11 with H catheters and 2 out of 9 with L catheters had complications (P<.005, all P values by Fisher's exact test). The major complication was renal infarction, occurring in 7 animals with H, 1g catheters and in no animals with L, 1g catheters(P=.005). 9 animals with H, 1g catheters and 2 with L, 1g catheters had aortic thrombosis(P=.021), which was minimal in the L, 1g group. In contrast to H. 1g catheters, the 10(3H, 7L)with catheters for ≤ 5 days had only minimal aortic thrombosis in 2(L), (P<.005). Neither the osmolarity of the fluid infused nor the presence of septicemia were related to complications. 6/21 had positive blood cultures at sacrifice. Our data indicate that in rabbits L catheters are safer than H ones, complications are time related in H catheters, and that osmolarity of infusate is not related to complications. If applied to the human neonate the data suggest umbilical artery catheters should be placed L, H catheters should be removed as soon as possible, and although caution is urged, it may be safe to give 20%D in L catheters.

Summary: Twenty pregnant rabbits were studied in pairs. Half were given cortisol subcutaneously on days 24. 25, and 26 of gestation in dosage of 2 nig/kg/day. Half served as controls and received saline. The fetal lungs were studied on the 27th day of gestation by incubating lung slices in the presence of [6-14C]glucose. Glucose consumption significantly increased in the tissues from animals treated with cortisol, 17.61 ± 5.56 (SD) μmol/g wet lung versus 14.28 ± 5.78 (SD) μmol/g in the controls (P < 0.05). The glycogen content of tissues treated with cortisol was significantly reduced compared to the controls, 2.42 ± 0.97 (SD) mg/g wet lung versus 3.81 ± 1.05 (SD) mg/g (P < 0.05). Treatment with cortisol resulted in significantly enhanced incorporation of the 14C label into glycogen and phosphatidl choline (Tables 3 and 4). These data suggest that glucocorticoids affect fetal lung phosphatidyl choline production by promoting glycogenolysis and increasing glucose incorporation into phosphatidyl choline. Speculation: Diminished glycogen content of the fetal lung in the latter part of gestation may reflect increasing utilization for phosphatidyl choline synthesis. Adenosine 3′,-5′-monophosphate (cyclic AMP) increases which occur after glucocorticoid administration may be responsible for activation of glycogen phosphorylases in the lung as they are in the liver. If insulin inhibits glycogenolysis in the lung as it does in the liver, insulin may inhibit phosphatidyl choline synthesis in the lung by preventing glycogen and glucose From serving as precursors.