Lium B, Aasen A O, Saugstad O D, Guldvog I, Nordstoga K, Amundsen E
Acta Pathol Microbiol Immunol Scand A. 1982 Mar;90(2):113-23. doi: 10.1111/j.1699-0463.1982.tb00071_90a.x.
The ultrastructure of developing lung lesions in two groups of dogs exposed to a combination of haemorrhagic hypotension and liver trauma was studied with particular attention to changes at the alveolar level and lung micro-vessels. Lung samples were obtained every four hours and at collapse in one group and 12 hrs after initiation of the trauma in the other. An interstitial oedema was recognized in biopsies obtained 4 hrs after initiation of the trauma, and before marked lesions were observed at the ultrastructural level in endothelial cells. Endothelial damage was, however, evident in biopsies obtained at 8 hrs and at collapse. Aggregates of degranulated and degenerated leucocytes and platelets were occasionally found to obstruct respiratory capillaries together with erythrocytes, some of which seemed to be haemolysing. A considerable amount of protein-rich oedema, cellular debris and fibrinoid material was found in alveolar lumina at collapse. The present experiments indicate that increased vascular permeability in lung micro-vessels is of importance for the development of the characteristic lesions seen in shock lung. Possible pathogenetic mechanisms, initiating the lung lesions, are discussed with special emphasis on the significance of kinin activation and the presence of polymorphonuclear leucocytes and microthrombi.
研究了两组遭受出血性低血压和肝创伤联合作用的犬肺脏病变的超微结构,特别关注肺泡水平和肺微血管的变化。一组每4小时取一次肺组织样本,直至肺塌陷;另一组在创伤开始后12小时取肺组织样本。在创伤开始后4小时获取的活检样本中可识别出间质性水肿,此时在内皮细胞的超微结构水平上尚未观察到明显病变。然而,在8小时获取的活检样本以及肺塌陷时的样本中,内皮损伤明显。偶尔会发现脱颗粒和变性的白细胞及血小板聚集体与红细胞一起阻塞呼吸性毛细血管,其中一些红细胞似乎正在溶血。在肺塌陷时,肺泡腔内发现了大量富含蛋白质的水肿液、细胞碎片和类纤维蛋白物质。本实验表明,肺微血管血管通透性增加对于休克肺中所见特征性病变的发展具有重要意义。讨论了引发肺病变的可能发病机制,特别强调了激肽激活以及多形核白细胞和微血栓存在的意义。