Partial liquid ventilation leads to clinical improvement and survival in some infants with severe respiratory distress syndrome who are not predicted to survive.

No abstract

We are interested in determining whether premature birth alters expression of counterregulatory cytokines which modulate lung inflammation. Production of proinflammatory cytokines tumor necrosis factor alpha. IL-1 beta, and IL-8 is regulated in part by the antiinflammatory cytokine IL-10. For preterm newborns with hyaline membrane disease, deficiencies in the ability of lung macrophages to express antiinflammatory cytokines may predispose to chronic lung inflammation. We compared the expression of pro- and antiinflammatory cytokines at the mRNA and protein level in the lungs of preterm and term newborns with acute respiratory failure from hyaline membrane disease or meconium aspiration syndrome. Four sequential bronchoalveolar lavage (BAL) samples were obtained during the first 96 h of life from all patients. All patients rapidly developed an influx of neutrophils and macrophages. Over time, cell populations in both groups became relatively enriched with macrophages. The expression of proinflammatory cytokine mRNA and/or protein was present in all samples from both patient groups. In contrast, IL-10 mRNA was undetectable in most of the cell samples from preterm infants and present in the majority of cell samples from term infants. IL-10 concentrations were undetectable in lavage fluid from preterm infants with higher levels in a few of the BAL samples from term infants. These studies demonstrate that 1) IL-10 mRNA and protein expression by lung inflammatory cells is related to gestational age and 2) during the first 96 h of life neutrophil cell counts and IL-8 expression decrease in BAL from term infants, but remain unchanged in BAL samples from preterm infants.

In this study, 12 male baboons were delivered by hysterotomy at 75% of gestation. The development of a nonlethal baboon model permitted a study of lung growth and development in long-term survivors. Control animals were ventilated with clinically appropriate oxygen for the 21 d study period. BPD animals were ventilated with PPV and an FIO2 of 1.0 for 7 d, followed by an FIO2 of 0.8 for 14 d. They survived for 33 wk, at which time a right lower lobe lobectomy was performed. Controls showed normal well-alveolated lungs, whereas BPD lungs showed enlarged airspaces focally, nonclassifiable as alveoli, alveolar ducts, or respiratory bronchioles. Volume densities of alveoli were decreased significantly (p = 0.0009), and enlarged airspaces were significantly increased (p = 0.0003) in the BPD group compared with controls. Alveolar counts verified a significant decrease in alveoli (p = 0.004), and the internal surface area was significantly decreased (p = 0.05) in BPD treated animals compared with controls. These data document that a mild to moderate BPD lesion results in a significant and permanent loss of alveoli and a significant increase in enlarged, unclassifiable airspaces, which together result in a decreased total internal surface area in baboons that survive with their disease.