Riede U N, Joachim H, Hassenstein J, Costabel U, Sandritter W, Augustin P, Mittermayer C
Pathol Res Pract. 1978 May;162(1):41-72. doi: 10.1016/S0344-0338(78)80130-7.
Interstitial edema in the alveolar septa is the first morphologically recognisable change to be observed in cases of shock. It is brought about by the altered function of the membranes of the damaged epithelium and endothelium in the alveolar wall. At the same time there is an impairment of gaseous exchange, which is rendered more difficult by the exudative process in the interstitium. Pari passu with these events there is injury to the cells of both the alveolar epithelium and the alveolar capillary endothelium. Both these processes are still reversible. The point of irreversibility appears to be reached--so far as time is concerned--at the end of the first week, after which the injurious effects on the cell are established, since the thin alveolar wall necessary for the exchange of gases becomes overgrown with bulky alveocytes (Tpye II), and the fibroblasts in thealveolar interstitium push the capillaries away from the surface of the alveolus. In most of the advanced cases of shock this process of thickening of the alveolar wall exceeds the critical value, and respiratory exchange is so impaired that satisfactory functioning of the lungs is no longer possible.
肺泡间隔的间质水肿是休克病例中首先在形态学上可识别的变化。它是由肺泡壁受损上皮和内皮细胞膜功能改变引起的。与此同时，气体交换受损，间质中的渗出过程使其更加困难。与这些事件同时发生的是肺泡上皮细胞和肺泡毛细血管内皮细胞均受到损伤。这两个过程仍然是可逆的。就时间而言，不可逆点似乎在第一周结束时达到，此后对细胞的损伤作用得以确立，因为气体交换所需的薄肺泡壁被大量的肺泡细胞（II型）过度生长，并且肺泡间质中的成纤维细胞将毛细血管推离肺泡表面。在大多数晚期休克病例中，肺泡壁增厚的这个过程超过临界值，呼吸交换受损严重，以至于肺不再能正常发挥功能。
