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Background: Surfactant lavage has been used to remove meconium debris in meconium aspiration syndrome (MAS), but the influence of surfactant lavage on pro-inflammatory cytokines and cellular apoptosis is unclear. The aim of this study was to investigate the response of pro-inflammatory cytokine and the influence on alveolar cellular apoptosis using therapeutic bronchoalveolar lavage with diluted surfactant to treat MAS. Methods: Twelve newborn piglets were anesthetized, intubated via tracheostomy, and artificially ventilated. MAS was induced by intratracheal instillation of 3–5 mL/kg of 20% human meconium. The piglets were then randomly assigned to a surfactant lavage group ( n= 6) or a control group ( n= 6). Piglets in the lavage group received bronchoalveolar lavage with 30 mL/kg diluted surfactant (5 mg/mL) in two aliquots. Cardiopulmonary parameters were monitored continuously. Serum was obtained hourly to measure concentrations of pro-inflammatory cytokines, including interleukin (IL)-Iβ, IL-6, and tumor necrosis factor α. Lung tissue was histologically examined after experiments, and terminal deoxynucleotidyl transferase-mediated nick-end labeling assay for apoptotic cell death was also performed. Results: The animals in the lavage group displayed significantly better gas exchange and lower serum concentrations of IL-1β than the animals in the control group ( P < 0.05). The number of apoptotic cells in lung tissues was significantly lower in the lavage group than the control group, and also in the nondependent than the dependent site. Conclusion: Therapeutic surfactant lavage improves oxygenation, decreases production of systemic pro-inflammatory cytokine IL-1β, and alleviates the severity of lung cell apoptosis in newborn piglets with experimentally-induced MAS. [ABSTRACT FROM AUTHOR]

Background: The physical-chemical properties of perfluorochemical (PFC) liquids have been shown to influence physiological and cellular responses during partial liquid ventilation (PLV). The aim of this study is to compare the relationship between patho-physiological endpoints and the physical properties of three PFC liquids used in treating acute lung injury. Methods: A total of 18 juvenile rabbits were randomized into conventional mechanical ventilation or PLV groups after lung saline lavages. Three PFC liquids, including Flutec perfluoro-1,3,5-trimethylcyclohexane (PP4; vapor pressure, 28.8 mmHg at 37°C), Perfluorodecalin (PFD; vapor pressure, 13.6 mmHg at 37°C), and Perflubron (PFB; vapor pressure, 10.4 mmHg at 37°C) were used for PLV with no replacement for 4 h. A thermal detector was used to measure PFC loss rate. Physiological measurements and evaporative loss rate of PFC were done every 30 min, and lung histology was examined. Results: The mean evaporative loss rate was significantly higher in the PP4 group (4.75 ± 0.24 mL/kg per h) than in either the PFD (1.43 ± 0.11 mL/kg per h) or the PFB (1.18 ± 0.05 mL/kg per h) group ( P < 0.05). The oxygenation of PFD and PFB was maintained good for 4 h, however, the PP4 group showed a fast deterioration since 2 h post-treatment due to fast dropping of the residual PP4 amount in lungs. Histology showed good alveolar integrity in the PFD and PFB groups. Conclusions: The effects of PLV are directly influenced by the evaporative property of the PFC liquid. With no replacement over 4 h, PLV effects could be maintained with utilizing a PFC liquid with low, rather than high, vapor pressure. PFC with high vapor pressure has a high loss rate and low residual volume that causes poor maintenance on oxygenation during PLV. Therefore, measuring PFC loss rate is important in future studies and clinical application of PLV. [ABSTRACT FROM AUTHOR]

The article offers information on acute respiratory failure in different origins that continues to be a major reason of morbidity and mortality. It mentions that meconium aspiration syndrome (MAS) is a common cause of severe respiratory failure in term infants. It further informs that bronchopulmonary dysplasia (BPD) or chronic lung disease (CLD) continues to be a major cause of neonatal morbidity.