Meconium aspiration syndrome (MAS) is related, in part, to exudative lung injury causing surfactant inhibition and pulmonary dysfunction. We evaluated the effect of intratracheal (IT) surfactant replacement (Survanta, Ross Laboratories) and recombinant human Cu-Zn superoxide dismutase (SOD) in a rat model of meconium (mec) injury. Intubated adult rats (400-500gm), ventilated with room air, received IT mec (.625ml/kg of 60mg/ml, n=5) or saline(1.6ml/kg, n=6). Three groups received mec then either 100mg/kg Survanta(Surv) after 15 min (n=4), or 5mg/kg SOD after 35min (n=5) or both Surv then SOD (n=3). All groups were ventilated for 60min, extubated to room air and at 24 hours (correlating with maximal injury) dynamic lung compliance (Cdyn, ml/cmH2O/kg) was measured and bronchoalveolar lavage (BAL) obtained. The mean±SE of BAL total protein (Protein, ug/ml), surfactant phospholipid (PL,ug/ml) and surfactant protein (SP-A, B, ratio to saline group) by immuno dot-blot and Western analysis were:Table Compared to saline animals, mec animals demonstrated lower Cdyn (1.2±33 vs..74±.17, respectively, p<0.05), which did not improve with Surv or SOD. In this model, Surv or SOD, alone or in combination, did not prevent exudative lung injury, or improve pulmonary mechanics. Surv alone increased PL and SP-A, while Surv with SOD resulted in even greater increases. We speculate that Surv therapy after mec injury may increase alveolar surfactant, and this effect may be accentuated by combined therapy with SOD.

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