Domenici-Lombardo L, Adembri C, Consalvo M, Forzini R, Meucci M, Romagnoli P, Novelli G P
Department of Human Anatomy and Histology, University of Florence, Italy.
Int J Exp Pathol. 1995 Oct;76(5):381-90.
To clarify the evolution of acute lung injury induced by endotoxin, the progression of lung damage in 26 rats submitted to intratracheal instillation of 5 mg/kg body weight endotoxin was examined by blood gas analysis, computerized tomography, light and electron microscopy. Hypoxaemia, hypercapnia, acidosis and inhomogeneous bilateral infiltrates developed gradually within 48 hours. Monocytes appeared within blood capillaries and the instertitium by 12 hours after treatment, then migrated into alveoli and underwent progressive differentiation into macrophages by 24 hours after treatment. Granulocytes were found within blood capillaries at an early stage, but outside capillaries only at 48 hours. Hyperplasia of type II pneumocytes and hypertrophy of interstitial fibroblasts also occurred at 48 hours. These data suggest that the pathogenesis of endotoxin induced pulmonary injury proceeds through an early phase of granulocyte migration inside capillaries and monocyte extravasation, an intermediate phase of monocyte differentiation into macrophages inside alveoli and a late phase of diffuse infiltration of alveoli by newly differentiated macrophages and late-extravasated neutrophils.
为阐明内毒素诱导的急性肺损伤的演变过程，通过血气分析、计算机断层扫描、光镜和电镜检查，对26只经气管内滴注5mg/kg体重内毒素的大鼠的肺损伤进展情况进行了研究。低氧血症、高碳酸血症、酸中毒和双侧不均匀浸润在48小时内逐渐出现。治疗后12小时，单核细胞出现在毛细血管和间质内，然后迁移到肺泡，并在治疗后24小时逐渐分化为巨噬细胞。粒细胞在早期出现在毛细血管内，但仅在48小时出现在毛细血管外。48小时时还出现了II型肺泡上皮细胞增生和间质成纤维细胞肥大。这些数据表明，内毒素诱导的肺损伤的发病机制经历了一个早期阶段，即粒细胞在毛细血管内迁移和单核细胞外渗；一个中间阶段，即单核细胞在肺泡内分化为巨噬细胞；以及一个晚期阶段，即新分化的巨噬细胞和晚期外渗的中性粒细胞对肺泡进行弥漫性浸润。
