FAILURE OF ACUTE PERINATAL ASPHYXIA OR MECONIUM ASPIRATION TO PRODUCEPERSISTENT PULMONARY-HYPERTENSION IN A NEONATAL BABOON MODEL

OBJECTIVE: Our purpose was to determine whether perinatal asphyxia or meconium aspiration, or both, can produce the physiologic and histolog ic pulmonary vascular changes associated with the meconium aspiration syndrome. STUDY DESIGN: Twenty neonatal baboons were studied in four g roups: 1, control; 2, meconium aspiration; 3, asphyxia (intermittent c ord compression); and 4, asphyxia with meconium aspiration, Animals we re ventilated for 24 hours under ketamine, diazepam, and pancuronium. Data were analyzed by means of mixed model analysis of measures. RESUL TS: Meconium significantly impaired oxygenation (p < 0.001), whereas c oncurrent asphyxia moderated this effect (p < 0.034), Meconium also in creased the need for ventilatory support (p < 0.002). No animal had pe rsistent pulmonary hypertension; neither systemic nor pulmonary systol ic pressures differed statistically between the groups. No animal show ed evidence of abnormal pulmonary arteriolar muscularization. CONCLUSI ON: Sublethal perinatal asphyxia or meconium aspiration were insuffici ent to produce either the physiologic or histologic changes of severe meconium aspiration syndrome. It is unlikely that intrapartum fetal di stress alone can produce this syndrome in human neonates.