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目的：建立内毒素诱导大鼠急性肺损伤的模型并筛选出敏感检测指标。方法：90 只wistar 大鼠随机分为10 组，其中9 组以气管内滴注内毒素（Lipopolysaccharide, LPS）建立大鼠急性肺损伤（Acute lung injury, ALI）模型，另一组作为空白对照组。观察造模8、12、24、36、48、72、96、120 h后的肺泡灌洗液（BALF）中肿瘤坏死因子-alpha（TNF-alpha）、白介素-6（IL-6）水平、肺组织的病理形态学变化、12h 造模组与空白组的BALF中的多形核白细胞(PMN)百分比和蛋白浓度。结果：造模后BALF中的TNF-alpha、IL-6 的浓度随时间延长显著升高且均在24 h达到峰值（P＜0.01）；肺组织病理损伤也逐渐加重，12 h已出现明显的肺泡损伤、肺水肿、炎性细胞浸润等病变；12 h 模型组BALF中PMN 百分比和蛋白浓度较空白对照组显著增加（P＜0.01）。结论：在该实验条件下，气管内滴注LPS 8 mg/kg，12 h后即可建立ALI模型，可通过检测BALF中的TNF-alpha、IL-6浓度及肺组织的病变程度等指标进行模型评价。

英文摘要:

Objective:To build the model of lipopolysaccharide-induced acute lung injury in rats and Screen the sensitive detection index.Methods:90 wistar rats were randomly divided into 10 groups, among which 9 groups of rats were used to establish the model of ALI by intratracheal administration of LPS, and the other group was used as blank control group. The level of TNF-alpha, IL-6 in bronchoalveolar lavage fluid (BALF) and histopathological changes in lung tissue would be tested after modeling for 8, 12, 24, 36, 48, 72, 96 and 120 h; The percentage of neutrophils and the concentration of protein exudation in BALF were detected in 12 h model group and the blank control group.Results:The level of TNF-alpha, IL-6 in BALF significantly increased with time and reached its peak value at 24 h after LPS administration (P< 0.01); Histologic examination of Lung gradually aggravated, alveolar structure damaged, pulmonary edema and inflammatory cells infiltration appeared in the 12 h model group. Compared with the blank group the percentage of PMN and protein concentration in BALF of 12 h model group increased obviously (P<0.01).Conclusion:Under the experimental conditions, ALI model could be established after intratracheal instillation of LPS 12 h and we would evaluate the model by detecting the level of TNF-alpha, and IL-6 in BALF and observing the histopathological changes in lung tissue.

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