1、 The Normal Alveolus and the Injured Alveolus in the Acute Phase of ALI and ARDS. In the acute phase, sloughing of both the bronchial and alveolar epithelial cells, the formation of protein-rich hyaline membranes on the denuded basement membrane.Neutrophils adhering to the injured capillary endothel
2、ium and marginating through the interstitium into the air space.(3)In the air space, an alveloar macrophage is secreting cytokines, IL-1, 6, 8, 10 and TNF-a, which act locally to stimulate chemotaxis and activate neutrophils. Macrophages also secrete other cytokines, including IL-1, 6, 10. IL-1 can
3、also stimulate the production of extracellular matrix by fibroblasts. (4)Neutrophils can release oxidants, proteases, LTs, and other proinflammatory molecules, such as PAF. A number of antiinflammatory mediators are also present in the alveolar milieu, including IL-1receptor antagonist, soluble TNF
4、receptor, autoantibodies against IL-8, and cytokines such as IL-10 and 11 (not shown). (5)The influx of protein-rich edema fluid into the alveolus has led to the inactivation of surfactant. MIF denotes macrophage inhibitory factor.Mechanisms in the Resolution of ALI and ARDS. On the left side of the
5、 alveolus, the alveolar epithelium is being repopulated by the proliferation and differentiation of alveolar type II cells. Resorption of alveolar edema fluid is shown at the base of the alveolus, with sodium and chloride being transported through the apical membrane of type II cells. Sodium is take
6、n up by the epithelial sodium channel (ENaC) and through the basolateral membrane of type II cells by the sodium pump (Na+/K+ATPase). The relevant pathways for chloride transport are unclear. Water is shown moving through water channels, the aquaporins, located primarily on type I cells. Some water
7、may also cross by a paracellular route. Soluble protein is probably cleared primarily by paracellular diffusion and secondarily by endocytosis by alveolar epithelial cells. Macrophages remove insoluble protein and apoptotic neutrophils by phagocytosis. On the right side of the alveolus, the gradual
8、remodeling and resolution of intraalveolar and interstitial granulation tissue and fibrosis are shown.（硬化）（硬化）Lung lavage cytokines after 2 h of mechanical ventilation in an ex vivo, nonperfused rat lung model. Each panel represents the results for a different cytokine. The X-axis in each panel repr
9、esents the ventilatory strategy used (C = control: VT = 7 mL/kg; PEEP = 3 cm H2O; = medium volume, high PEEP: VT = 15 mL/kg, PEEP = 10 cm H2O; = medium volume, zero PEEP: VT = 15 mL/kg, PEEP = 0; = high volume, zero PEEP: VT = 40 mL/kg, PEEP = 0). ARDS病人BALF中SP-A水平降低，而血清水平明显增高,血清SP-A可作为预测ARDS发生的高危因素。 具ARDS高危因素病人,BALF抗IL-8/IL-8复合物含量越高，发生ARDS几率越大，死亡率越高。与肺泡中PMN浓度正相关。 ALI病人肺水肿液及血浆中含量数倍于正常人，HT156可以作为肺泡上皮损伤标记物，用于预测ALI发生。单克隆抗体单克隆抗体 IgMTNF-、IL-1 、IL-6、IL-8白细胞粘附抗体白细胞粘附抗体 CD11/CD18单克隆抗体单克隆抗体
