Nasal ventilation alters mesenchymal cell turnover and improves alveolarization in preterm lambs. Am J Respir Crit Care Med 2008 Aug 15;178(4):407-18
Date
06/17/2008Pubmed ID
18556628Pubmed Central ID
PMC2542442DOI
10.1164/rccm.200802-359OCScopus ID
2-s2.0-48949083712 (requires institutional sign-in at Scopus site) 68 CitationsAbstract
RATIONALE: Bronchopulmonary dysplasia (BPD) is a frequent cause of morbidity in preterm infants that is characterized by prolonged need for ventilatory support in an intensive care environment. BPD is characterized histopathologically by persistently thick, cellular distal airspace walls. In normally developing lungs, by comparison, remodeling of the immature parenchymal architecture is characterized by thinning of the future alveolar walls, a process predicated on cell loss through apoptosis.
OBJECTIVES: We hypothesized that minimizing lung injury, using high-frequency nasal ventilation to provide positive distending pressure with minimal assisted tidal volume displacement, would increase apoptosis and decrease proliferation among mesenchymal cells in the distal airspace walls compared with a conventional mode of support (intermittent mandatory ventilation).
METHODS: Accordingly, we compared two groups of preterm lambs: one group managed by high-frequency nasal ventilation and a second group managed by intermittent mandatory ventilation. Each group was maintained for 3 days.
MEASUREMENTS AND MAIN RESULTS: Oxygenation and ventilation targets were sustained with lower airway pressures and less supplemental oxygen in the high-frequency nasal ventilation group, in which alveolarization progressed. Thinning of the distal airspace walls was accompanied by more apoptosis, and less proliferation, among mesenchymal cells of the high-frequency nasal ventilation group, based on morphometric, protein abundance, and mRNA expression indices of apoptosis and proliferation.
CONCLUSIONS: Our study shows that high-frequency nasal ventilation preserves the balance between mesenchymal cell apoptosis and proliferation in the distal airspace walls, such that alveolarization progresses.
Author List
Reyburn B, Li M, Metcalfe DB, Kroll NJ, Alvord J, Wint A, Dahl MJ, Sun J, Dong L, Wang ZM, Callaway C, McKnight RA, Moyer-Mileur L, Yoder BA, Null DM, Lane RH, Albertine KHMESH terms used to index this publication - Major topics in bold
AnimalsAnimals, Newborn
Apoptosis
Bronchopulmonary Dysplasia
Caspase 3
Cell Division
Continuous Positive Airway Pressure
Gestational Age
High-Frequency Ventilation
Humans
Infant, Newborn
Intermittent Positive-Pressure Ventilation
Mesoderm
Oxygen
Proliferating Cell Nuclear Antigen
Pulmonary Alveoli
Sheep
Tidal Volume
