Abstract

The pathophysiology of meconium aspiration syndrome (MAS) is attributed in part to the development of lung surfactant dysfunction in vivo. Meconium (the first excrement of the newborn) and its components are responsible for development of lung surfactant dysfunction. In this study, the effect of meconium and its components on the surface activity of spread surfactant monolayers was evaluated using Wilhelmy balance at physiological temperature and pH. The effect of meconium on adsorption, airway patency and ultrastructure of liposomes made of various surfactant lipids was also evaluated. Significant inhibition of DPPC monolayer surface activity was observed on addition of meconium, its organic and aqueous phase extracts. All the surfactant lipid mixtures including DPPC attained significantly higher minimum surface tensions (between 12 and 20 mN/m) and lowered monolayer compressibility modulus in presence of meconium suggestive of surfactant monolayer fluidization. Meconium reduced the airway patency and affected the adsorption of DPPC liposomes and was associated with altered ultrastructure of DPPC liposomes. Meconium caused the maximum inhibitory effect on DPPC:PE and DPPC:PG and the least inhibitory effects on DPPC:POPC and DPPC:CHOL in terms of minimum surface tensions. All the surfactants were equally inhibited in terms of airway patency. These findings have implications for the differential inhibition of different surfactants in MAS and for the designing of surfactants that are resistant to meconium inhibition.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call