The Labeling of Lung Phosphatidylchohne in Premature Rabbits

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Abstract

Summary

Lung phosphatidylcholine metabolism was studied in vivo in premature rabbits delivered by cesarean section as early in gestation as compatible with prolonged viability (28.9 days). The newborn rabbits initially required supplemental oxygen and had respiratory distress. The amount of phosphatidylcholine isolated from the lung parenchyma changed little over the first 3 days of life, while phosphatidylcholine in the alveolar wash increased in 3 days from 0.05–3.1 μmol/50 g animal. The phosphatidylcholine of the lungs of the premature rabbits was pulse labeled with isotopically labeled palmitic acid, choline, and phosphate given to the pregnant does 10 min before delivery of the newborns. After the initial incorporation period, the total amount of radioactive precursor (palmitic acid, choline, or 32P) incorporated into lung phosphatidylcholine did not change for a period of 4 days. Labeled phosphatidylcholine was detected initially in alveolar wash 3 hr after administration of the three precursors and continued to accumulate for many hours. The biological half-life values for lung and alveolar phosphatidylcholine indicated that phosphatidylcholine was turning over very slowly. However, if the effect of dilution on the measured specific activity caused by phosphatidylcholine accumulation was considered, virtually no labeled alveolar or lung phosphatidylcholine disappeared during the 3–4 days of these observations. These results with premature newborn rabbits were similar to those for term newborn rabbits, but different from similar measurements made in the adult rabbit.

Speculation

Premature newborn rabbits are unable to deliver newly synthesized phosphatidylcholine rapidly to the alveolar space in the hours immediately after birth. These newborn animals seem to depend on stored phosphatidylcholine to maintain alveolar stability at birth. Continuous de novo synthesis then produces a slow accumulation of phosphatidylcholine in the alveolar space. If these results can be generalized to the premature human with respiratory distress syndrome, phosphatidylcholine synthesized shortly before or after birth would not be expected to mitigate alveolar collapse. A considerable period of respiratory support would be anticipated before large amounts of newly synthesized alveolar phosphatidylcholine would become available for the maintenance of alveolar stability. However, any phosphatidylcholine present may have a very long biological half-life as increasing amounts of alveolar phosphatidylcholine accumulate during the recovery period.

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