MECONIUM ASPIRATION SYNDROME - PHYSIOLOGICAL AND INFLAMMATORY CHANGESIN A NEWBORN PIGLET MODEL

In order to evaluate further the physiological and inflammatory change s of meconium aspiration syndrome (MAS), 25 newborn piglets (1-2 days old, 1.5 +/- 0.4 kg) were studied. Piglets were briefly ventilated wit h 100 % oxygen and then received an intratracheal bolus of 3 mL/kg of a 20% suspension of human meconium. They were then further ventilated, keeping Pa(CO2) at approximately 40 torr and Pa(O2)) at 70 torr durin g 4, 12, 24, and 48 h studies. Pulmonary function studies and tracheal aspirates were obtained at time zero and serially throughout the stud y. Bronchoalveolar lavage was performed at the end of the study to exa mine endogenous surfactant function. Control piglets received 3 mL/kg of intratracheal saline and were then ventilated for 48 h at an inspir ed oxygen concentration and mean airway pressure matched to the meconi um treated group (to control for the effects of hyperoxia and barotrau ma on the lung). MAS caused acute decreases in gas exchange and dynami c lung compliance, which returned toward baseline by 48 h (P < 0.001, ANOVA). Tracheal aspirate absolute neutrophil count, neutrophil chemot actic activity, albumin, and total protein concentrations also increas ed significantly over time (P < 0.001). Endogenous surfactant function appeared to be significantly inhibited by the meconium. All variables of lung injury were significantly higher in the meconium group compar ed to the saline control group over the 48 h study. Newborn piglets pr ovide a clinically relevant model of MAS, demonstrating physiological and inflammatory changes with apparent alterations in endogenous surfa ctant function. Effective therapies for MAS may require interventions directed at all of these components of lung injury. (C) 1993 Wiley-Lis s, Inc.