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Modern neonatal care has made remarkable progress to improve the outcome of premature infants. However, the syndrome of chronic neonatal lung disease (nCLD), defined by prolonged oxygen requirement following premature birth, continues to affect nearly one in two infants born before 28 weeks completed gestation. Since the introduction of exogenous surfactant replacement and lung protective ventilation strategies the phenotype of nCLD has changed. nCLD is now a subtle disease of disrupted lung development, yet oxygen dependance—without a universally agreed on oxygen saturation target—remains the core diagnostic feature.1 It is remarkable that despite the advances of modern neonatology little progress has been made discriminating physiological subtypes within nCLD.
While the physiology of oxygenation is well understood as a combined function of the alveolar and vascular lung compartments, research of the pathophysiology of nCLD—clearly a multifactorial process—has largely focused on the alveolus. A disproportionally high interest has been given to the pre/postnatal proinflammatory milieu, maladaptive parenchymal development and ‘alveolar simplification’. However, equally important to oxygenation is the appropriate development of the pulmonary vascular bed. As such, hypoxaemia and oxygen-dependance may be the consequence of multiple pathologies of disrupted lung development, including pulmonary vascular disease.
The ‘vascular hypothesis’ regards interruption of pulmonary vasculature development as a main factor of aberrant alveolar development.2 Autopsy findings, …
Contributors AG and JT contributed equally to drafting and editing the manuscript.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests AG has no competing interests. JT performs preclinical research funded by Chiesi Farmaceutici S.p.A.
Provenance and peer review Commissioned; externally peer reviewed.