Increased surface tension (ST) forces at the gas-liquid interface are responsible, in part, for the pulmonary dysfunction associated with aspiration of meconium (Mec). Parenchymal lung injury from Mec, however, may alter elastic lung properties and compromise mechanics independent of ST forces. To investigate the pathophysiology of Mec injury, we instilled 32mg dry weight of human Mec in 0.5 ml saline (NS), or NS intratracheally in 400-450 gm adult rats, followed by 30 minutes of mechanical ventilation with room air. Following extubation, the animals spontaneously breathed room air for 16 hours, a period we previously demonstrated to concur with maximal exudative lung injury. After 16 hours, dynamic compliance (Cdyn, ml/cmH2O/kg) and total pulmonary resistance (cmH2O/l/s) were measured using an esophageal balloon and pnuemotachography. Excised, degassed lungs were then inflated with NS, to generate static liquid filled pressure-volume curves(Cstat, ml/cmH2O/kg). Separate Mec and NS animals had lungs excised and lavaged (BAL) with NS. Total protein (Protein, μg/ml) and electrophoresis(PAGE) were performed on cell free lavage fluid. The mean±SE values were: Table PAGE demonstrated a predominance of serum proteins in BAL, confirming endothelial dysfunction. Even with the elimination of ST forces by liquid filling, injured lungs demonstrated heightened elastic forces and lung compliance remained decreased. These results indicate airway and parenchymal dysfunction associated with meconium induced lung injury. This suggests that in Mec injury, surfactant inhibition accounts for only part of the diminished mechanics, and that interstitial lung changes may significantly and independently affect lung mechanics.
