Pulmonary vascular endothelial cells (ECs) line the surface of the lung vasculature and accommodate the various levels of blood flow. Pulmonary endothelium is a critical regulator of vascular homeostasis by inhibiting coagulation of the blood. The ECs bind tissue factor pathway inhibitors (TFPI), modulate hemostasis with opposing effects such as antiplatelet, anticoagulant and fibrinolytic properties. Lung endothelium regulates synthesis and metabolism of vasoactive compounds such as nitric oxide and endothelin-1, both potent regulators of vascular tone. Cytokines, chemokines, interleukins, adhesion molecules, and growth factors can be secreted by pulmonary ECs with positive and adverse effects. Pulmonary endothelium exhibits heterogeneity with diverse expression of molecules and specific differences in signaling induced by various infections such as Gram-positive bacteria. The distinction of macro or microvascular endothelium occurs from the larger vessels to small capillaries in the lung alveoli system. Lectin-binding patterns discriminate between pulmonary artery and pulmonary microvascular capillary endothelium. The lung is one of the body’s organs with the highest expression of vascular endothelial growth factor that stimulates small vessel formation of the microvascular endothelium. Acute respiratory distress syndrome and acute chest syndrome in sickle cell disease are two prototypes of devastating diseases caused by pulmonary EC dysfunction.
Part of the book: Endothelial Dysfunction