The pulmonary endothelium, poised at the interface between air, blood, and tissue, provides both rapid and sustained responses to local and systemic perturbations. This complex vascular structure occupies a surface area of 120m2 and forms the intimal lining of the pulmonary arterial, venous, and capillary beds with a single continuous layer of endothelial cells (ECs) linked to each other by specialized junctions (1). The alveolar endothelium is intimately related to the alveolar epithelium both in terms of anatomic location and functions that include oxygen (O2), carbon dioxide, water and solute transport, and barrier regulation; disruption of barrier functions of the alveolar capillary membrane is an early and critical event in the pathogenesis of acute respiratory distress syndrome (ARDS) (see later and Box 128.1). Alveolar epithelial function, which is beyond the scope of this chapter, has recently been reviewed (2).
Once thought of as passive, semipermeable conduits for nutrient and O2 delivery – and in the lungs, contributing to separation of blood from air (1) (Box 128.1) – ECs were dismissed as structural bystanders with little or no capacity to respond to activating signals with changes in phenotype or function (3). During the 1950s, electron microscopic observations that ECs contain secretory granules, together with ongoing physiological studies of EC–leukocyte interactions, implicated the endothelium as an active participant in both physiological and pathophysiological responses to injury and inflammation (4–6). Subsequent studies clearly demonstrated that, even under normal physiological conditions, the “quiescent” endothelium is far from inactive and is involved in multiple homeostatic functions. These include, but are not limited to, cellular and nutrient trafficking, angiogenesis and vasculogenesis, regulation of vascular tone, and maintenance of blood fluidity and vascular barrier function (3–7).
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