No abstract

SummaryPhosphatidylglycerol (PG) was absent from lung effluent in 41 infants with respiratory distress syndrome of the newborn (RDS), whereas effluent from healthy control subjects of similar gestational age contained this phospholipid (4.9 + 2.4% of lipidphosphorus (P), n = 32). Control infants of 28 weeks of gestation or less with various respiratory disturbances other than RDS also had low PG (0.2 + 0.2% of lipid-P, n = 5). In RDS surfactant complex often could be isolated from the airways using differential and density gradient centrifugation. The material thus obtained had promipent phosphatidylinositol (PI) (13.6 * 2.8% of lipid-P, n = 6), but no PG. Of those 1 8 infants who had such surfactant even in the early stages of RDS, 1 3 were 35 weeks of gestation or more, 3 were offspring of diabetic mothers, and 2 had severe perinatal asphyxia. In healthy control subjects PG sometimes appeared first within an hour of birth, but in RDS PG did not appear until recovery from RDS.In RDS type I1 (transient tachypnea of the newborn) PG in lung effluent also was abnormally low (1.3 * 0.6% of lipid-P, n = 5) and PI was correspondingly prominent (9.7 + 3.6% of lipid-P, n = 5), indicating immaturity of surfactant similar to RDS. Surfactant with PG and PI has superior surface-active properties compared to that containing PI, but no PG. Surfactant without PG does not seem to stabilize the alveoli of the newborn as well as does surfactant with PG. The failure of PG appearance following birth therefore may precipitate RDS, especially beyond 35 weeks of gestation.

SummaryThe lung lecithin of term newborn rabbits was labeled by injecting the lecithin precursors palmitic acid and cholme into the pregnant doe shortly before delivery of the newborn rabbits by cesarean section. The newborn lungs were lavaged to yield an alveolar wash lecithin sample and the tissue was homogenized and fractionated into lamellar body and microsomal fractions by differential and density gradient centrifugation. Lecithin was isolated from the lung parenchyma, microsomes, lamellar bodies, and alveolar wash by two-dimensional thin layer chromatography, and the specific activity of the lecithin in each fraction was determined. Comes are presented showing the time of appearance of the radioactive lecithin in each lecithin fraction. The apparent biological half-life of lecithin in each fraction was measured.The specific activity of lecithin was high in microsomal fractions soon after palmitic acid or choline administration. The lamellar body fraction was free of radioactive lecithin for 3 hr, and maximal specific activity of lamellar body lecithin was reached only after 20 hr. The appearance of radioactive alveolar lecithin followed a curve very similar to that of the lecithin in the lamellar body fraction.The apparent half-life of lung parenchymal lecithin from newborn lung labeled with palmitic acid was 57 hr, whereas the apparent half-life of alveolar lecithin was 136 hr. The lecithin in lung and alveolar wash labeled with choline had a longer halflife than did lecithin labeled with palmitic acid. Measurements of lecithin appearance and apparent half-life are compared to similar measurements in adult rabbits. SpeculationThe striking characteristics of newborn lung lecithin are the 3-hr lag before the appearance in the alveolus of de novo synthesized lecithin, the prolonged time (20 hr) before maximal specific activity of alveolar lecithin is achieved, and the very long! apparent half-life of alveolar lecithin. If these measurements are applicable to other term and premature mammals, they must rely entirely on lecithin stored in anticipation of birth to maintain alveolar stability at birth. The long lag before significant lecithin synthesized de novo can reach the alveolar space precludes synthesis contributing to alveolar stability until many hours after birth. The recovery from the respiratory distress syndrome may not depend on maturation of the ability to synthesize lecithin; rather, the prolonged recovery phase may reflect the long times required for appreciable quantities of de novo synthesized lecithin to reach the alveolar space. However, once alveolar stability is achieved, short interruptions of lecithin synthesis, by reversible acidosis, for example, should not cause respiratory distress mediated by lecithin deficiency.The times required for lecithin synthesis and appearance in the alveolar space and the biological half-life of alveolar surfactant lecithin are measurements essential to an understanding of surfactant physiology. These measurements have been made in the adult rat using sever...