Background: Treatment with surfactant (S) decreases lung injury in paralyzed, mechanically ventilated animals. The use of nasal continuous positive airway pressure (CPAP) as an alternative to mechanical ventilation may further improve acute pulmonary outcomes. Objectives: To evaluate the effect of surfactant (+S, –S) and synchronized intermittent mandatory ventilation (SIMV) on lung morphology and inflammatory markers in 24 spontaneously breathing piglets treated with CPAP or SIMV after saline lavage-induced lung injury. Methods: After induction of lung injury, animals were randomized to CPAP–S, CPAP+S or SIMV+S and treated for 4 h. Physiologic parameters were continuously monitored. After treatment, animals were euthanized and lungs fixed. Bronchoalveolar lavage (BAL) samples were collected for neutrophil count and H2O2. Results: No physiologic differences were noted. BAL fluid from CPAP–S animals contained more neutrophils and more neutrophil H2O2 than fluid from the SIMV+S or CPAP+S groups (p < 0.05 or greater). Pathologic injury scores were higher in dependent lung regions from CPAP groups (p < 0.05). Injury pattern scores showed greater dependent alveolar inflammation in all (p < 0.02), with more dependent atelectasis in the CPAP groups (p < 0.01). Morphometrics showed less total open alveolar air space in nondependent regions of the SIMV+S group compared to CPAP groups (p < 0.001). Dependent regions showed less total open alveolar air space compared to nondependent regions in the CPAP groups (p < 0.001). Conclusions: Animals treated with surfactant prior to CPAP or SIMV had less acute lung injury. SIMV+S animals had less open air space in nondependent regions. This suggests, during early ventilatory support, surfactant administration may modulate pulmonary inflammation. CPAP alone without surfactant may not provide optimal pulmonary protection. The addition of mechanical breaths may alter and add to injury.
We hypothesized that animals treated with nasal continuous positive airway pressure following surfactant administration (NCPAP+S) would have decreased inflammatory markers and pathologic lung injury compared with those treated with synchronized intermittent mandatory ventilation following surfactant administration (SIMV+S) or NCPAP without surfactant administration (NCPAP-S).MethodsWe compared NCPAP+S, SIMV+S, and NCPAP-S in spontaneously breathing piglets with saline lavage induced lung injury (PaO2 of 80-100 torr in FIO2 1.0). Animals were randomized to NCPAP (n=7), SIMV+S (n=8), or to NCPAP+S (n=10) and were treated for 4 hours. Settings were PIP 20, PEEP 5, rate 20, VT 8ml/kg. NCPAP was initiated at 5cmH2O. Oxygen was adjusted to maintain PaO2 of 80-100 torr. Physiologic parameters and arterial blood gases were continuously monitored and recorded hourly. Bronchoalveolar lavage (BAL) samples were collected for neutrophil count and H2O2 after 4 hours treatment. Animals were euthanized and lungs were fixed for histopathologic scoring and morphometric analysis. Physiologic data were analyzed using ANOVA for repeated measures. Neutrophil count and H2O2 were analyzed using ANOVA.ResultsNo physiologic differences were noted between groups. BAL fluid from NCPAP-S piglets contained significantly more neutrophils than those from the SIMV+S group (p≤0.05) with a similar trend in the CPAP+S group (p≤0.17). BAL cells from the SIMV+S and NCPAP+S groups contained significantly less H2O2 than cells from the NCPAP-S group (p≤0.01 and 0.03 respectively). Morphometric analysis showed more total open alveolar airspace in the dorsal regions in the NCPAP+S group compared to the NCPAP-S group (p≤0.01) with a similar trend in the SIMV+S vs NCPAP-S groups (p≤0.09). Conversely, ventral regions showed more total open alveolar airspace in the NCPAP-S group compared to NCPAP+S or SIMV+S (p≤0.05 and 0.01 respectively).ConclusionAnimals treated with surfactant prior to initiation of respiratory support had less evidence of acute lung injury after treatment for 4 hours. Morphometric data suggest surfactant administration results in regionally dependent lung expansion.
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