Schnells G, Voigt W H, Redl H, Schlag G, Glatzl A
Acta Chir Scand Suppl. 1980;499:9-20.
Lung biopsies were taken from patients during the course of post-traumatic respiratory insufficiency, from 3 hours to 19 days after the onset of shock. Electron-microscopic investigations revealed that the initial phases of cellular damaged were followed by both endothelial and epithelial changes, including atelectasis, lymphatic dilation, and interstitial as well as interalveolar fibrin extravasation. Interstitial edema and extravascular migration of granulocytes, lymphocytes and mast cells are followed by fibroblastic proliferation and, as an end result, fibrosis of the alveolar septa. As a result, fibroblasts replace capillaries at the surface, where gas exchange takes place. The capillaries are forced into the depths of the interstitial tissues. At the same time, the alveolar surface becomes covered with thick-walled proliferating epithelial cell layers, which also renders gas exchange increasingly difficult. Lung function is thereby reduced.
在创伤后呼吸功能不全病程中，于休克发生后3小时至19天对患者进行肺活检。电子显微镜检查显示，细胞损伤的初始阶段之后出现内皮和上皮变化，包括肺不张、淋巴管扩张、间质以及肺泡内纤维蛋白外渗。间质水肿以及粒细胞、淋巴细胞和肥大细胞的血管外迁移之后是成纤维细胞增殖，最终导致肺泡间隔纤维化。结果，成纤维细胞取代了进行气体交换的表面毛细血管。毛细血管被挤入间质组织深处。与此同时，肺泡表面被厚壁增殖的上皮细胞层覆盖，这也使气体交换越来越困难。肺功能因此降低。
