Pulmonary endothelial cell pathobiology: implications for acute lung injury.

Pulmonary endothelial cells form a continuous monolayer on the luminal surface of the lung vasculature. Until the mid-1970s, the pulmonary endothelium was felt to provide little more than a passive surface for the exchange of gases, water, macromolecules, and some cell traffic. Recent evidence indicates that the pulmonary endothelium is a metabolically active surface, which provides a regulatory interface for the continual processing of blood-borne vasoactive molecules, plays an active role in hemostasis and immunologic and inflammatory events, regulates vascular tone, and interacts with inflammatory cells and neighboring vascular cell types. These metabolic properties are both constitutive and capable of being induced in response to stimuli or injury. Virtually any agent that causes pulmonary endothelial cell injury will lead to impairments in the functional metabolic properties of these cells, resulting in alterations in hemodynamics, hemofluidity, permeability, gas exchange, and intercellular signaling. The net result in the lung is often the clinical picture of acute lung injury with respiratory distress, refractory hypoxemia, diffuse alveolar infiltrates, and respiratory failure.