To test the hypothesis whether lung inflammatory reaction play a role in the development of PPHN in newborn piglet with MAS, we have conducted a study on 35 newborn piglets (age 1-3 days, wt 2.4-3.5 kg): 13 were randomly assigned to MAS (Gr I) (intratracheal bolus of 3 ml/kg of 20% suspension of human meconium with amniotic fluid), 15 to MAS but pretreated with dexamethasone (Gr II) (0.25 mg/kg/dose q.12.h for 4 doses) and 7 as control (Gr III)(intratracheal saline). A bullon thermodilution catheter was inserted to measure pulm, arterial pressure (PAP), wedge pressure and cardiac output. All piglets were intubated and ventilated to maintain blood gases at appropriate levels. Serial tracheal aspirates were obtained for Leukotriene (LTB4 D4) thromboxane (TxB2) and 6-Keto PGF1a measured by RIA. (* p<.05 **p<.01, compared with Gr III control) Table

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Gr I and II had sig. higher mPAP than Gr III from 20′ to 2-16hr and at d-3, and d-4. Tracheal aspirate cytokines were comparable between the groups until 24-48h when Gr I and Gr II had sign higher LTB4. D4, 6-Keto PGF1a than Gr III. The used of dexamethasone (Gr II) reduced LTB4, D4, 6-Keto PGF1a on d-4 but did not alter mPAP. We concluded: 1) MAS produces a biphasic elevation of mPAP; early course may be related to airway obstruction and hypoxia while the late course to inflammation. The use of dexamethasone does not alter this course.