phosphorus-radioisotopes and Respiratory-Distress-Syndrome--Newborn

Surfactant protein A (SP-A) metabolism was studied in vivo in 33 preterm ventilated lambs at 138 +/- 1 days gestational age by measuring recoveries of exogenously administered surfactant containing both radiolabeled SP-A and labeled saturated phosphatidylcholine (Sat PC) given via the trachea at birth. Endogenously secreted SP-A was also labeled with [35S]methionine and followed over 24 h. The exogenously labeled SP-A left the alveolar pool more rapidly than did Sat PC over the first 5 h of life (P less than 0.05), and both exogenously labeled SP-A and Sat PC were detected within lamellar bodies by 2 h, indicating uptake from the airspaces. The quantity of SP-A in alveolar washes increased about twofold from birth to 5 h of age, whereas alveolar Sat PC pools were constant over 24 h. The SP-A endogenously labeled with [35S]methionine was recovered at highest specific activities in the alveolar washes at 10 and 45 min after birth with no labeled SP-A detectable in lamellar body fractions until 2 h. The curve for endogenous SP-A labeling of lamellar bodies was similar to that for exogenous labeling, indicating that SP-A was initially secreted by a pathway independent of lamellar bodies with subsequent SP-A labeling of lamellar bodies. The kinetics of SP-A metabolism were very different than for Sat PC in preterm lambs.

Topics: Animals; Animals, Newborn; Cesarean Section; Chromatography, Affinity; Gestational Age; Humans; Infant, Newborn; Kinetics; Lung; Methionine; Phosphatidylcholines; Phosphorus Radioisotopes; Proteolipids; Pulmonary Alveoli; Pulmonary Surfactant-Associated Protein A; Pulmonary Surfactant-Associated Proteins; Pulmonary Surfactants; Respiration, Artificial; Respiratory Distress Syndrome, Newborn; Sheep; Sulfur Radioisotopes; Tritium

Acute fetal asphyxia resulting from maternal blood loss and hypotension causes a reduction in the incorporation of precursors into disaturated phosphatidylcholine, the principal lipid in the pulmonary surfactant. Treatment of the maternal hypotension is associated with return of fetal lung DSPC synthesis to control levels by 72 hours.

Topics: Acidosis, Respiratory; Animals; Carbon Radioisotopes; Female; Fetal Hypoxia; Humans; Infant, Newborn; Lung; Palmitic Acids; Phosphates; Phosphatidylcholines; Phosphorus Radioisotopes; Pregnancy; Respiratory Distress Syndrome, Newborn; Sheep

Topics: Embolism, Fat; Enzyme Precursors; Humans; Infant, Newborn; Phosphatidylethanolamines; Phospholipases; Phospholipids; Phosphorus Radioisotopes; Pulmonary Alveoli; Pulmonary Surfactants; Respiratory Distress Syndrome, Newborn