The pathophysiology of the acute respiratory distress syndrome Donna L. Carden, J. Steven Alexander, Ronald B. George  Pathophysiology  Volume 5, Issue 1, Pages 1-13 (June 1998) DOI: 10.1016/S0928-4680(98)00004-2

Fig. 1 The alveolar–capillary membrane. This figure shows the anatomical structure of the alveolar–capillary membrane. The central alveolar airspace (A) is covered by type I (I) and type II alveolar epithelial cells (II), which together, cover the surface of the airspace. Within the alveolus and in contact with the alveolar epithelial cells, are alveolar macrophages (AM) which actively phagocytize bacteria and particulate matter entering the airspace. Immediately below the epithelial barrier is the basement membrane (BM), which is secreted by both endothelial and epithelial cells. Pulmonary endothelial cells (Endothelial cell), adjacent to the basement membrane, form the capillary network surrounding the airspace. Pathophysiology 1998 5, 1-13DOI: (10.1016/S0928-4680(98)00004-2)

Fig. 2 Ion and water transport through the alveolar epitheilal barrier. Water and ions are transported between the alveolar airspace and the capillary lumen by convective and osmotic forces created by the active transport of sodium (Na+) at the basolateral surface of type I alveolar epitheilal cells (left). The energy dependent pumping of sodium (Na+) from the type 1 cells to the interstitial space draws Na+ into the apical cell surface through amiloride-sensitive sodium channels. Water and chloride (Cl−) are convectively drawn into the cell by specialized channels, termed `aquaporins'. Pathophysiology 1998 5, 1-13DOI: (10.1016/S0928-4680(98)00004-2)

Fig. 3 Adhesion molecules on the alveolar capillary membrane. Several classes of adhesion molecules participate in the rolling, adhesion, diapedesis and alveolar trafficking of leukocytes in addition to altering the barrier function of the alveolar capillary membrane in ARDS. Initially, leukocytes roll on activated endothelial cells by forming a loose bond between neutrophil sialyl LewisA, fucosylated sialyl LewisX, PSGL-1 and endothelial cell P-selectin. The subsequent, firm adhesive contact between neutrophil CD11b/CD18 and endothelial cell ICAM-1 facilitates leukocyte migration across the endothelium into the interstitial space. During migration, neutrophils pass across endothelial and epithelial junctions containing cadherins and occludin. These membrane proteins may be transiently or permanently altered in ARDS. Finally, alveolar epithelium ICAM-1 may facilitate leukocyte trafficking and adhesion in the alveolar airspace. Pathophysiology 1998 5, 1-13DOI: (10.1016/S0928-4680(98)00004-2)

Fig. 4 Micrograph of intestinal ischemia-reperfusion elicited lung inflammation stained for ICAM-1 (blue), neutrophils (pink) and fluoroscein-labed albumin to delinate the vascular space (green). Systemic inflammation induces marked lung leukocyte retention, neutrophil-endothelial cell interaction and fluid and protein extravasation. Image courtesy of D. Carden, V. Specian and R. Specian. Pathophysiology 1998 5, 1-13DOI: (10.1016/S0928-4680(98)00004-2)