Strange C, Tomlinson J R, Wilson C, Harley R, Miller K S, Sahn S A
Department of Medicine, Medical University of South Carolina, Charleston 29425.
Exp Mol Pathol. 1989 Dec;51(3):205-19. doi: 10.1016/0014-4800(89)90020-8.
Models of pleural injury were established with intrapleural tetracycline, intrapleural carrageenan, and empyema in New Zealand White rabbits to evaluate histologically the pleural inflammatory response from 3 to 90 days. Both tetracycline and empyema models produced increases in the pleural connective tissue layers both above and below the fibroelastic membrane associated with angiogenesis and lymphangiogenesis. The influx of fibroblasts from the pleural surface into acellular fibrin strands formed adhesions between the visceral and the parietal pleurae. Injury to the mesothelial cell ranged from a cuboidal transition to total desquamation with the degree of mesothelial injury associated with the amount of fibrin adherence and the propensity toward fibrosis at 90 days. Intervention to promote the resolution of pleural inflammation without fibrosis should be directed toward preservation of the mesothelial surface, removal of pleural fibrin, and inhibition of fibroblast growth and chemotaxis.
通过向新西兰白兔胸腔内注射四环素、角叉菜胶和造成脓胸来建立胸膜损伤模型,以便从组织学角度评估3至90天内的胸膜炎症反应。四环素模型和脓胸模型均使纤维弹性膜上下的胸膜结缔组织层增加,伴有血管生成和淋巴管生成。成纤维细胞从胸膜表面流入无细胞纤维蛋白条索,在内脏胸膜和壁层胸膜之间形成粘连。间皮细胞损伤范围从立方形转变至完全脱屑,间皮损伤程度与90天时的纤维蛋白黏附量及纤维化倾向相关。促进胸膜炎症消退而不发生纤维化的干预措施应着眼于保护间皮表面、清除胸膜纤维蛋白以及抑制成纤维细胞生长和趋化性。