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：目的：探讨内毒素在急性肺损伤（ＡＬＩ）中的作用机制及大黄、地塞米松对ＡＬＩ的保护作用。方法：在Ｗｉｓｔａｒ大鼠舌下静脉注射内毒素（ＬＰＳ）复制ＡＬＩ动物模型。动物分为４组：ＬＰＳ致伤组，对照组（生理盐水），地塞米松治疗组，大黄治疗组。肉眼观察肺大体标本；普通光镜检查肺组织病理变化；电镜观察肺组织超微结构；测定ＡＬＩ的生物学指标：肺湿重与干重比，肺泡灌洗液中中性粒细胞比例和蛋白含量，肺泡通透指数和肺毛细血管通透性。结果：ＬＰＳ致伤组：大体见斑片状坏死；光镜下肺间质水肿，肺泡腔内可见大量红细胞渗出、中性粒细胞浸润和血浆蛋白渗出；电镜示肺血管内皮细胞损伤；肺湿重与干重比、肺泡灌洗液中中性粒细胞比例、蛋白含量及肺泡通透指数、肺毛细血管通透性均显著升高。地塞米松和大黄治疗组上述组织学检查结果均较ＬＰＳ组明显减轻，肺损伤的生物学指标均较ＬＰＳ组显著下降。结论：ＬＰＳ致ＡＬＩ的机制主要是直接损伤肺泡上皮和血管内皮细胞致肺泡毛细血管内皮屏障发生障碍，致血管通透性增加和中性粒细胞浸润。大黄及地塞米松对血管内皮和肺泡上皮具有保护作用。
OBJECTIVE: To investigate the mechanism of endotoxin in acute lung injury (ALI) and the protective effect of rhubarb and dexamethasone on ALI. METHODS: Endogenous toxin (LPS) was injected into the sublingual vein of Wistar rats to replicate ALI animal model. Animals were divided into 4 groups: LPS-induced injury group, control group (normal saline), dexamethasone treatment group, and rhubarb treatment group. The gross lung specimens were observed with naked eyes; pathological changes of the lungs were examined by ordinary light microscope; the ultrastructure of the lung tissues was observed by electron microscopy; and the biological indicators of ALI were measured: wet/dry weight ratio of lung, ratio of neutrophils in bronchoalveolar lavage fluid, and protein Content, alveolar permeability index and pulmonary capillary permeability. RESULTS: In the LPS-injured group, plaque necrosis was generally seen. Pulmonary interstitial edema was observed under light microscopy. Numerous erythrocytes exuded in the alveolar cavity, neutrophil infiltration, and plasma protein exudation were observed. Electron microscopy showed pulmonary vascular endothelial cell injury. Wet weight and dry weight ratio of lung, ratio of neutrophils in bronchoalveolar lavage fluid, protein content, alveolar permeability index, and pulmonary capillary permeability were significantly increased. Both the dexamethasone and rhubarb treatment groups significantly reduced the above histological findings compared with the LPS group. The biological parameters of lung injury were significantly lower than those of the LPS group. Conclusion: The mechanism of LPS-induced ALI is mainly to directly damage the alveolar capillary endothelial barrier caused by alveolar epithelium and vascular endothelial cells, resulting in increased vascular permeability and neutrophil infiltration. Rhubarb and dexamethasone have protective effects on vascular endothelium and alveolar epithelium.