The compliance of the respiratory system was determined at an average of 2.89 h (range 45 min – 8 h) after birth in 82 newborns who were retrospectively divided into group 1: healthy newborns (mean gestational age 37.1 weeks, range 30–41 weeks); group 2: newborns with respiratory distress (RD) needing no ventilatory support (mean gestational age 37.3 weeks, range 35–40 weeks); group 3: newborns with RD needing ventilatory support and surviving (mean gestational age 34.3 weeks, range 30 – 39 weeks), and group 4: newborns with RD who needed ventilatory support and died (mean gestational age 30’.8 weeks, range 28 – 37 weeks). Respiratory compliance was measured by the airway occlusion technique in spontaneously breathing babies and by injecting a known volume of gas into the closed airway system and measuring airway pressure in intubated babies. The difference in postnatal compliance was statistically significant (p < 0.01) in those four groups and was correlated with the severity of the disease in groups 2 and 3. In infants with RD, compliance was highly predictive for the need for ventilatory support (93% correct and 7% erroneous) and in infants with ventilatory support, for the mortality (83% correct and 17% erroneous). We conclude that postnatal compliance measurements are very useful to predict the course and outcome as well as to classify the severity of RD.

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.

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The C-reactive protein (CRP) concentration was determined in 25 infants whose mothers had presented with prolonged rupture of amniotic membranes (PROM) and/or amnionitis. CRP was positive (i.e. greater than or equal to 6 mg/l) within the first 6 hrs of life in 10 and negative in 15 infants. Clinically, all infants with positive CRP developed symptoms suggesting bacterial infection and both the absolute immature neutrophil counts as well as the ratio immature/total neutrophils were significantly higher in them on day 2 of life than in infants with negative CRP. Blood cultures were only positive in infants with positive CRP. Thus CRP can be regarded as an early marker for neonatal bacterial infection due to PROM and/or amnionitis.

Pregnant rats received betamethasone 0.02, 0.05, 0.10, or 0.20 mg/kg body weight/day or saline (controls) for three days before delivery of fetuses at day 19 of gestation. Dose related effects on morphology, dipalmitoyl phosphatidylcholine content, and phosphatidylcholine species composition of the fetal lungs were evaluated. Injection of 0.02 and 0.05 mg/kg body weight betamethasone resulted in cellular differentiation of some cells, but the increase in dipalmitoyl phosphatidylcholine content was not significant. Dosages of either 0.10 or 0.20 mg/kg body weight resulted in markedly accelerated organ differentiation, complete cytodifferentiation of type II cells, and markedly increased numbers of lamellar bodies per alveolar type II cell. Compared to the controls, maternal administration of 0.10 or 0.20 mg/kg betamethasone caused significant increases of both fetal lung dipalmitoyl phosphatidylcholine content, and the fraction of dipalmitoyl phosphatidylcholine of total phosphatidylcholine. None of the parameters differed between the groups that were treated with 0.10 or 0.20 mg/kg body weight betamethasone respectively. Diminution of lung DNA content was significant after treatment with betamethasone in doses of 0.05, 0.10, and 0.20 mg/kg body weight. The results of the present study suggest that maternal treatment with lower doses than those in common usage may be successful in prevention of respiratory distress syndrome, and that higher dosages do not confer any additional advantage.