Oxygen exposure in the newborn guinea pig lung lavage cell populations, chemotactic and elastase response: a possible relationship to neonatal bronchopulmonary dysplasia.

Neonatal guinea pig pulmonary response to oxygen exposure FiO2 greater than 0.9 resulted in an increase in total cell number in lung lavage. Alveolar macrophages initially increased within 48 h of exposure. Polymorphonuclear leukocytes and macrophages exceeded age-matched neonatal control values by 72 h of oxygen exposure. By 144 h of life, total inflammatory cell number still exceeded control cell populations. Chemotaxis of alveolar macrophages to N-formyl-methionyl-phenylalanine (1 x 10(-5) M) exceeded chemotaxis of air-exposed controls. Although initially depressed, by 72 h of FiO2 greater than 0.9 polymorphonuclear leukocyte chemotaxis increased 6-fold. Endogenous chemotactic peptides were demonstrated in lung lavage supernatant of oxygen-exposed neonatal guinea pigs. Elastase activity rose in oxygen exposed guinea pigs by 72 h of life. Lung lavage disaturated phosphatidylcholine in oxygen-exposed neonates exceeded control values 4-fold. In a preliminary study, lung effluent elastase activity was found to be increased in human neonates with respiratory distress syndrome over the first days of life compared to infants intubated but without lung disease. In infants developing bronchopulmonary dysplasia, tracheal aspirate protease activity remained greater than 10(-3) U for over 10 days and up to 5 weeks of age.