ABSTRACT
A single layer of mesenchymal-derived, nonfenestrated lung microvascular endothelial cells (ECs) serves as a semipermeable cellular barrier between the lung interstitium and the pulmonary circulation. The large surface area of the lung microvasculature is well suited for regulating multiple key biologic processes (including lung fluid balance and solute transport between vascular compartments). Since the pulmonary circulation receives the entire cardiac output, it is also well positioned to sense mechanical, chemical, and cellular injury by inhaled or circulating substances. During conditions of intense lung inflammation such as observed in acute lung injury (ALI) or acute respiratory distress syndrome (ARDS), the large surface area becomes a liability and provides the opportunity for profound vascular permeability and alveolar flooding, critical and defining features of common and devastating inflammatory lung disorders primarily caused by sepsis, pneumonia, and trauma (1,2).
