Riede U N, Mittermayer C, Friedburg H, Wybitul K, Sandritter W
Pathol Res Pract. 1979 Nov;165(3):269-86. doi: 10.1016/s0344-0338(79)80075-8.
In the initial phase of shock, edema spreads throughout the alveolar interstitium even before injury occurs in the alveolar epithelium and endothelium. The endothelium and the epithelium are damaged only subsequently, causing reduction in the average barrier thickness of the epithelium and the endothelium. A point of irreversibility is reached by the end of the first week. While early cell regeneration may be observed within the alveolar endothelium and epithelium, proliferation of fibroblasts and fibrosis of the alveolar wall occur in addition to edema which spreads within the interstitium. This widening of the gas exchange barrier may be considered as the anatomic substrate of respiratory insufficiency induced by shock. This enlargement continues up to the moment when thickening of the alveoli impedes satisfactory functioning of the lung, and, as consequence, threatens the life of the patient.
在休克的初始阶段，水肿甚至在肺泡上皮和内皮受损之前就已扩散至整个肺泡间质。内皮和上皮随后才会受损，导致上皮和内皮的平均屏障厚度减小。到第一周结束时就会达到不可逆点。虽然在肺泡内皮和上皮内可观察到早期细胞再生，但除了在间质内扩散的水肿外，肺泡壁的成纤维细胞增殖和纤维化也会发生。气体交换屏障的这种增宽可被视为休克诱发的呼吸功能不全的解剖学基础。这种扩大一直持续到肺泡增厚阻碍肺的正常功能，进而危及患者生命之时。
