cl lglyccrol \\‘;Is tletected ill none of the amniotic Huid sarnplr\, although 11011e of the baby baboons born at term developed hyaline membrane disease. Compared 10 Iluman amniotic fluid. fluid from baboons had much Iightel lecithin spots on the chromatograms, suggesting low colicentrations of lecithin, even at ter-m. Of the eigllt surfactants purihed from amniotic fluid obtained at term, none contained detectable amounts of phosphatidvlgiyc.erol, yet six of’ seven surfactants purified from products of lung lavage did contain phosphatidylglycerol. These I./S ratio data al-c quite similar to those previousl~, reported in baboons.’ Compared to human>. baboons have low L/S ratios at term as well as a suggestion of lower overall concentrations of lecithins. The absence of phosphatidylglycerol at term, similar to that observed in sheep, is of great interest. Three explanations are possible: (I ) Baboon fetuses produce no phosphatidylgfycerol; (2) phosphatidylglyterol is prcsent in amniotic Huicl but its concentration is too low to be detected; (3) phosphatidylglycerol is present in the lungs but is not excreted into the amniotic, fluid. The absence of ~~~losphatidylglvcer-ol in concentrated hutfactants purified from am~‘lioric Huid and its present< in surktants purified f.rom lung lavagc point to thr third explanation. These data have two implications for perinatal care and research. First, absence of phosphatidylglycerol in amniotic Huid should not be assumed to imply absence of phosphatidylgl~cerol in alveolar fluid. Second, since phosphatidylglycerol appears to be necessary to maintain alveolar stability, surfactants purified from amniotic fiuid should be tested for phosphatidylglycerol prior to use in trials ofsurfactant replacement. Furthet research into the mechanism of lecithin excretion into amniotic fluid is needed.