Part of the book: Bronchial Asthma
The successful transition from liquid to air breathing at birth is essential in mammalian lung development and the primary biological role of the hypothalamic-pituitary-adrenal axis. At this moment, the lung experiences a major environmental change in oxygen tension as the fluid that filled this organ in utero (pO2 ∼26) is rapidly replaced with ambient air during the first few breaths (pO2 ∼150). This change induces oxidant stress in the lung which is balanced by antioxidant genes that are induced in the late gestational fetal lung to protect against injury. These antioxidant genes impact distinct antioxidant molecules, including glutathione, which can regulate the level of redox stress in lung cells. Cells, such as the alveolar macrophage, are central for host defense and surfactant homeostasis at the newly established air-liquid surface. Yet they are prone to dysfunction with excessive oxidant stress and the newborn lung is susceptible to infection. And yet the rise in alveolar oxygen tension can also serve as a physiologic redox signal that initiates expression of genes that regulate postnatal lung development. Taken together, birth can be viewed as a natural experiment with hyperoxia where the birth process itself serves as an integrator for that level of redox stress that limits lung injury while activating genes required for postnatal lung development.
Part of the book: Respiratory Management of Newborns