Failure of acute perinatal asphyxia or meconium aspiration to produce persistent pulmonary hypertension in a neonatal baboon model

J. Devn Cornish, Gary L. Dreyer, Gary E. Snyder, Thomas J. Kuehl, Dale R. Gerstmann, Donald Null, Jacqueline J. Coalson, Robert A. deLemos

Research output: Contribution to journalArticle

26 Scopus citations


OBJECTIVE: Our purpose was to determine whether perinatal asphyxia or meconium aspiration, or both, can produce the physiologic and histologic pulmonary vascular changes associated with the meconium aspiration syndrome. STUDY DESIGN: Twenty neonatal baboons were studied in four groups: 1, control; 2, meconium aspiration; 3, asphyxia (intermittent cord compression); and 4, asphyxia with meconium aspiration. Animals were ventilated for 24 hours under ketamine, diazepam, and pancuronium. Data were analyzed by means of mixed model analysis of measures. RESULTS: Meconium significantly impaired oxygenation (p < 0.001), whereas concurrent asphyxia moderated this effect (p < 0.034). Meconium also increased the need for ventilatory support (p < 0.002). No animal had persistent pulmonary hypertension; neither systemic nor pulmonary systolic pressures differed statistically between the groups. No animal showed evidence of abnormal pulmonary arteriolar muscularization. CONCLUSION: Sublethal perinatal asphyxia or meconium aspiration were insufficient to produce either the physiologic or histologic changes of severe meconium aspiration syndrome. It is unlikely that intrapartum fetal distress alone can produce this syndrome in human neonates.

Original languageEnglish (US)
Pages (from-to)43-49
Number of pages7
JournalAmerican Journal of Obstetrics and Gynecology
Issue number1
StatePublished - Jan 1 1994
Externally publishedYes



  • acute intermittent asphyxia
  • baboon
  • meconium aspiration syndrome
  • persistent fetal circulation
  • Persistent pulmonary hypertension of the newborn

ASJC Scopus subject areas

  • Obstetrics and Gynecology

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