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Meconium aspiration syndrome (MAS) is a frequent cause of respiratory distress in neonates. Recent reports have suggested that surfactant dysfunction contributes to the pathophysiology of MAS and surfactant therapy improves oxygenation of infants with MAS. We evaluated the effect of bronchial lavage with surfactant solution in a rabbit model of meconium aspiration. All animals were given 5 mL/kg of a 20% slurry of human meconium into the endotracheal tube and mechanically ventilated. The animals were then divided into saline lavage (n = 5) or surfactant lavage (n = 5). Lavage was performed an hour after meconium instillation. After the lavage the total amount of meconium recovered was measured. Blood gas was monitored during the experiment. The amount of meconium recovered by saline lavage was 14%, and by surfactant lavage was 57%. The surfactant group had a significant improvement in gas exchange, whereas the saline group had no improvement. It was concluded that the lavage with surfactant solution effectively washed out meconium and improved gas exchange in rabbit model of MAS.

A serial determination of pulmonary surfactant apoprotein-A (SP-A) was made on tracheal aspirates from seven intubated infants with different types of respiratory failure in the first week of life. A two-site immunoassay with monoclonal antibodies was adopted to determine the SP-A concentration. The concentrations of albumin in the same samples were also assayed, and these data were expressed as the ratio of SP-A to albumin (SP-A/albumin ratio), and evaluated against clinical data such as the arterial-alveolar oxygen tension ratio (a/APO2) or ventilatory index. In infants with respiratory distress syndrome, the SP-A/albumin ratio was initially low, and increased gradually in the first few days of life with the improvement of a/APO2 and ventilatory index. The complication of pulmonary hemorrhage due to patent ductus arteriosus (PDA) resulted in a temporary decrease in the ratio. The infant with transient tachypnea of the newborn showed higher concentration from the first day of life and, in the course of PDA without pulmonary hemorrhage, the ratio did not decrease. The cases of congenital pneumonia showed the SP-A/albumin ratio remaining low while the infection was evident. These data suggest that the SP-A/albumin ratio of the tracheal aspirate can be used for the quantitative and qualitative evaluation of endogenous pulmonary surfactant in newborn infants with different respiratory disorders.

In order to evaluate the influence of maternal anti-HLA antibody on neonatal thrombocytopenia, clinical features and maternal anti-HLA antibody of three groups of infants (19 thrombocytopenic and low birth weight, 27 nonthrombocytopenic and low birth weight, and 80 healthy full-term) were investigated. The incidence of positive maternal anti-HLA antibodies in the three groups was 73.7%, 29.6% and 27.5%, respectively. Thrombocytopenia in small-for-gestational-age (SGA) infants was closely related to the presence of maternal anti-HLA antibodies. Among 20 SGA infants (11 thrombocytopenic, 9 non-thrombocytopenic), anti-HLA antibody was detected in 10 mothers (90.9%) of thrombocytopenic SGA infants, while it was positive in only one mother (11.1%) of nonthrombocytopenic SGA infants. Investigation of the SGA infants revealed that in those whose mothers were sensitized to HLA antigen, not only the platelet count but also the leukocyte and lymphocyte counts in the first week of life were significantly lower than in infants whose mothers were not sensitized. The results suggest that the presence of maternal anti-HLA antibody is a cause of neonatal thrombocytopenia especially in SGA infants.