Summary: Administration of L-caniitine or betamethasone to pregnant rats failed to increase either the total phospholipid or dipalmitoylphosphatidylcholine (DPPC) contents in foetal rat lungs on the 20th day of j gestation, eompared to cpntrols. The combined administration of betamethasone (0.3 mg/kg) and L-carnitine ; (80 mg/kg) resulted in a pronounced increase of dipalmitoylphosphatidylcholine (7.8 ±2.5 mg/g dry weight) j coinpared with the control group (5.4 ± 1.8 mg/g dry weight), and compared with the groups receiving betamethasone (5.9 ±1.9 mg/g dry weight) or L-carnitine (5.6 + 1.5 mg/g dry weight) alone. The proportion of dipalmitoylphosphatidylcholine in the phosphatidylcholine species increased from 20.9 ±2.1% in the foetal lungs of the control group to 22.6 ± 5.0% in the L-carnitine group, to 24.3 + 3.3% (p < 0.01) in the betämethasone-i-carnitine (20 mg/kg) group, to 25.2 ± 3.5% (p < 0.01) in the betamethasone group, to 27.1 + 2.6% (p < 0.01) in the betamethasone-L-carnitine (40 mg/kg) group, and to 28.4 ± 3.7% (p < 0.01) in the betamethasone-L^carnitine (80 mg/kg) group, while the palmitic acid portion in the phosphatidylcholine fatty acids was nearly unchanged. A pronounced increase of palmitoyl-myristoyl phosphatidylcholine (PC-30), the second disaturated phosphatidylcholine species present in lungs in significant amounts beside dipalmitoylphosphatidylcholine, was noted only in betamethasone treated animals. Furthermore, after betamethasone and betamethasone^carnitine treatment, a significant diminution (p < 0.01) of the proportion of palmitoyl-palmitoleyl phosphatidylcholine (16 : 0/16 : l-PC) in the phosphatidylcholine species was demonstrated. After L-carnitine and betamethasone-L-carnitine treatment a significant increase (p < 0.01) of the Proportion of palmitoleyl-palmitoyl phosphatidylcholine (16 :1/16 : 0-PC) in the phosphatidylcholine species was found. Administration of L-carnitine to pregnant rats (either alone or in combination with betamethasone) resulted in a significant elevation (p < 0.01) of the carnitine levels in the foetal lungs to approximately twice those of the controls. The results suggest that a betamethasone-L-carnitine combination has both additive effects and effects specific for the combination, neither of which are found when carnitine or betamethasone is administered alone.

Pregnant rats received 0.10 or 0.20 mg/kg body weight betamethasone, or 100 mg/kg body weight L-carnitine, or L-carnitine 100 mg/kg plus betamethasone 0.05 or 0.10 mg/kg body weight, or saline (controls) for three days before delivery of foetuses at day 19 of gestation. Dose-related effects on the dipalmitoyl phosphatidylcholine content and the phosphatidylcholine species composition of foetal and maternal lungs were determined. Betamethasone (0.10 and 0.20 mg/kg) or L-carnitine (100 mg/kg) significantly increased (p < 0.05) the dipalmitoyl phosphatidylcholine content in the foetal lungs, while only small changes were found in relative terms. Combinations of betamethasone (0.05 or 0.10 mg/kg) with L-carnitine (100 mg/kg) also significantly increased the dipalmitoyl phosphatidylcholine content of the foetal lungs above control values (p < 0.01) and above the values achieved with betamethasone alone (p < 0.05). In the maternal lungs a significant increase of the dipalmitoyl phosphatidylcholine content above the control values was only found after treatment with betamethasone-carnitine combinations, whereas compared with the foetal lung the relative increase of dipalmitoyl phosphatidylcholine as a fraction of total phosphatidylcholine was more pronounced after betamethasone treatment. The gas Chromatographie method used separates two monoenoic phosphatidylcholine species with 32 carbon atoms in the acyl residues. These two phosphatidylcholine species showed striking differences between adult and foetal lungs. Palmitoleyl palmitoyl phosphatidylcholine predominates in the maternal lung, whereas palmitoyl palmitoleyl phosphatidylcholine is the major monoenoic phosphatidylcholine species with 32 carbon atoms in the foetal lung. These two species were not affected in maternal or foetal lung by betamethasone or L-carnitine treatment. In contrast, after treatment with betamethasone-carnitine combinations, a significant increase of the fraction of palmitoyl palmitoleyl phosphatidylcholine was found in foetal but not in the maternal lung. The results of the present study demonstrate that maternal glucocorticoid and carnitine treatment affects the maternal as well as the foetal lung but with different effects on the dipalmitoyl phosphatidylcholine content and phosphatidylcholine species composition.

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