Pulmonary Vascular Remodeling by High Oxygen

Abstract

As an organ of gas exchange, the lung and its vasculature function optimally at the level of oxygen in air. This chapter reviews the effect of breathing a higher than normal atmospheric level of oxygen on the vasculature of the lung. The earth's atmosphere contains 20.99% oxygen, and at this concentration efficiently sustains life (cell respiration and metabolism). Studies have demonstrated the toxic effects of breathing a high oxygen tension on lung tissue, mainly in response to normobaric hyperoxia, as differences began to emerge between the response of an organ, or tissue, and how the oxygen is administered. Higher than normal partial pressures of oxygen can be administered in an atmosphere of reduced total barometric pressure (hypobaric hyperoxia), at sea level (normobaric hyperoxia), or at a total partial pressure of oxygen greater than the total barometric pressure at sea level (hyperbaric hyperoxia). Studies show that breathing high oxygen injures the adult lung's vasculature, while prolonged exposure to hyperbaric hyperoxia induces vasculitis, with endothelial cell proliferation and hyalinization of the walls of large and small pulmonary arteries. This chapter discusses the potential mechanisms involved in pulmonary vascular remodeling in response to cycles of breathing high oxygen, or high oxygen and then air, discusses the observations that would improve understanding of the pathobiology of vascular changes that characterize the adult lung in pulmonary hypertension, and highlights the striking degree of plasticity of the lung's vascular bed in matching vascular density to the ambient alveolar oxygen tension.