Interaction between pulmonary surfactant and vernix: a potential mechanism for induction of amniotic fluid turbidity.

The development of amniotic fluid turbidity during the third trimester is a known marker of fetal lung maturity. We hypothesized that this turbidity results from detachment of vernix caseosa from the fetal skin secondary to interaction with pulmonary-derived phospholipids in the amniotic fluid. To test this hypothesis, we exposed vernix to bovine-derived pulmonary surfactant over a physiologically relevant concentration range. Ten milligrams of vernix was evenly applied to the interior walls of 1.5-mL polypropylene microfuge tubes. Surfactant phospholipids were added to the tubes followed by slow rotation at 37 degrees C overnight. The liquid was decanted and spectrophotometrically analyzed at 650 nm to detect solution turbidity due to vernix detachment and/or emulsification. Increasing concentrations of surfactant phospholipids produced a dose-dependent increase in solution turbidity. A phospholipid mixture closely approximating natural pulmonary surfactant but devoid of surfactant-associated proteins yielded no increase. In other studies, the flow properties of vernix were studied in a Haake flow rheometer at 23 degrees C and 37 degrees C. There was a marked temperature-dependent effect with lower stress required to elicit flow at 37 degrees C compared with 23 degrees C. This temperature dependence was also demonstrated in the turbidity assay with a 124% increase in turbidity at body temperature compared with room temperature. We conclude that under in vitro conditions, pulmonary surfactant interacts with vernix resulting in detachment from a solid phase support. We speculate that in utero, this phenomenon contributes to the increase in amniotic fluid turbidity that is observed near term.