From: Pulmonary Atelectasis:A Pathogenic Perioperative Entity Anesthes. 2005;102(4):838-854. Figure Legend: Fig. 1. (  A  and  B  ) In normal lungs (  A  ), the alveolar inflation and vascular perfusion are associated with low stress and are not injurious. Two separate barriers form the alveolar–capillary barrier, the microvascular endothelium, and the alveolar epithelium. In contrast, with atelectasis (  B  ), alveolar inflation and deflation may be heterogeneous, and the resulting airway stress causes epithelial injury. Because the blood vessels are compressed, perfusion may be traumatic because of flow-induced disruption of the microvascular endothelium. Both epithelial and endothelial injury may initiate or propagate lung injury. This figure depicts the advanced stage of lung injury caused by atelectasis. The initial injury is simple collapse of alveoli. However, with time, this leads to an inflammatory reaction. As the derecruited lungs cause epithelial injury and loss of epithelial integrity, both type I and type II alveolar cells are damaged. Injury to type II cells disrupts normal epithelial fluid transport, impairing the removal of edema fluid from the alveolar space. In addition to collapse, derecruited lungs also become fluid filled. Neutrophils adhere to the injured capillary endothelium and migrate through the interstitium into the alveolar airspace. In the airspace, alveolar macrophages secrete cytokines, interleukin (IL)-1, -6, -8, and -10, and tumor necrosis factor (TNF)-α, which act locally to stimulate chemotaxis and activate neutrophils. IL-1 can also stimulate the production of extracellular matrix by fibroblasts. Neutrophils can release oxidants, proteases, leukotrienes, and other proinflammatory molecules, such as platelet-activating factor (PAF). MIF = macrophage inhibitory factor.  Date of download: 12/30/2017 Copyright © 2017 American Society of Anesthesiologists. All rights reserved.