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ARDS基本的病理生理变化是自身免疫系统介导的肺泡毛细血管膜损伤。细胞动力学研究表明,血管中50～60%中性粒细胞储存在肺血管床,存在“着边”和沿血管内膜“滚动”现象。由于肺毛细血管的物理约束力,其绝大部分滞留在肺毛细血管。当失血性或感染性休克时,肺血流成慢,肺血管容量进一步扩大。随之,炎性调节因子介导的粘附机制增加中性粒细胞聚集。参与内毒素反应的细胞因子主要有TNF-α、Il-1、Il-8和Il-6。炎性内皮细胞增加其表面内皮细胞白细胞粘附分子(ELAM),细胞间粘附分子(ICAM),以及细胞颗粒膜蛋白140(GTMP-140)。未受刺激的中性粒细胞表面存在植物凝血素粘附分子(LECAM),活化的中性粒细胞则表达整合素(Intergrins)。整合素是由普通β_2单位或一组不同的18链(CD18)与不同的α链(CDlla、CDllb、CDllc)共价结合所组成。在其表面形成三个不同的异构二聚体。一般中性粒细胞粘附和
The basic pathophysiological changes of ARDS are the autoimmune system-mediated alveolar capillary membrane damage. Cytokinetic studies have shown that 50 to 60% of neutrophils in the blood vessels are stored in the pulmonary vascular bed, and there is a “rolling edge” and “rolling” phenomenon along the intima of blood vessels. Due to the physical binding of pulmonary capillaries, most of them remain in the pulmonary capillaries. When hemorrhagic or septic shock, pulmonary blood flow slows down, pulmonary vascular capacity to further expand. Subsequently, the inflammatory regulatory factor-mediated adhesion mechanisms increase neutrophil aggregation. The cytokines involved in endotoxin response are mainly TNF-α, Il-1, Il-8 and Il-6. Inflammatory endothelial cells increase their surface endothelial cell leukocyte adhesion molecule (ELAM), intercellular adhesion molecule (ICAM), and granulocyte membrane protein 140 (GTMP-140). Proliferating cell adhesion molecules (LECAM) are present on unstimulated neutrophils, and activated neutrophils express Intergrins. Integrins are composed of either ordinary β_2 units or a set of different 18-chain (CD18) covalently bound to different α-chains (CDlla, CD11b, CD11c). Three different heterogeneous dimers form on its surface. General neutrophil adhesion and