The pathogenesis of neonatal
meconium aspiration syndrome (MAS) may involve inactivation of endogenous
surfactant, and data from clinical pilot studies indicate that treatment with exogenous
surfactant may alleviate
respiratory failure in babies with MAS. We studied ventilation efficiency
after treatment with a modified porcine
surfactant in experimental
meconium aspiration. Adult rats were anesthetized and tracheotomized, and received via a tracheal
cannula from 4 to 6 ml/kg
body weight of a saline
suspension of human meconium (25 mg [dry weight]/ml). After 30 min of ventilation with 100%
oxygen, the animals were in
respiratory failure, with dynamic lung-thorax compliance < 0.5 ml/cm H2O/kg and PaO2 < 8 kPa (60 mm Hg). Animals were then allocated to: (1) immediate treatment with
surfactant (200 mg/kg); (2) treatment with
surfactant (200 mg/kg 3 h later; or (3) a control group not receiving
surfactant. All animals were ventilated for 6 h with variable FIO2 and peak inspiratory/
positive end-expiratory pressure (PIP/PEEP). In the control group, six of 12 animals died of
respiratory failure with
hypoxemia and
acidosis despite ventilation with 100%
oxygen and high mean airway pressure (> 20 cm H2O). The lungs of all animals in this group showed severe
atelectasis, influx of neutrophils,
edema, and hyaline membranes. In contrast, animals allocated to immediate or late
surfactant treatment had lower mortality (one of seven and two of eight, respectively), a reduction of
oxygen supply by 30%, and a decrease in mean airway pressure of 3 to 4 cm H2O. This was associated with a > 50% increase in static lung volume at 40 cm H2O inflation and 10 cm H2O deflation pressure and improved alveolar expansion in histologic sections. Hyaline membranes tended to be less prominent in
surfactant-treated animals than in controls. We conclude that both early and late treatment with
surfactant is effective in this animal model of MAS.