Jobe A H, Ikegami M
Pulmonary Biology, Children's Hospital Medical Center, Cincinnati, OH 45229-3039, USA.
Proc Assoc Am Physicians. 1998 Nov-Dec;110(6):489-95.
This brief review will emphasize four interconnected pathways that can lead to functional abnormalities of surfactant that contribute to lung mechanics and gas exchange abnormalities in acute lung injury. Type II cells, the cells that make and secrete all of the lipids and proteins in surfactant, can be injured, resulting in disruption of metabolic pathways. The normal alveolar conversion of surfactant from active to inactive forms can accelerate with lung injury to deplete the active alveolar pool of surfactant. Alveolar-capillary damage from mechanical ventilation or cytokines will result in interstitial and alveolar edema, and alveolar edema can inhibit surfactant function by a variety of mechanisms. The host defense systems in the lung include macrophages and surfactant protein-A (SP-A). Injury can result in SP-A depletion, macrophage activation, and migration of activated granulocytes into the lungs with release of inflammatory cytokines, oxidants, and proteases that can interfere with surfactant function.
本简要综述将着重介绍四条相互关联的途径，这些途径可导致表面活性剂功能异常，进而导致急性肺损伤时肺力学和气体交换异常。II型细胞是合成和分泌表面活性剂中所有脂质和蛋白质的细胞，可能会受到损伤，从而导致代谢途径中断。随着肺损伤，表面活性剂从活性形式向非活性形式的正常肺泡转化会加速，从而耗尽肺泡内活性表面活性剂池。机械通气或细胞因子引起的肺泡-毛细血管损伤会导致间质和肺泡水肿，而肺泡水肿可通过多种机制抑制表面活性剂功能。肺中的宿主防御系统包括巨噬细胞和表面活性剂蛋白A（SP-A）。损伤可导致SP-A耗竭、巨噬细胞活化以及活化的粒细胞迁移至肺内，并释放可干扰表面活性剂功能的炎性细胞因子、氧化剂和蛋白酶。
