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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-α(TNF-α)、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-α、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-α、IL-6浓度及肺组织的病变程度等指标进行模型评价。
Objective: To establish a model of endotoxin-induced acute lung injury in rats and screen out sensitive detection indexes. Methods: Ninety wistar rats were randomly divided into 10 groups. 9 rats were subjected to acute lung injury (ALI) model by endotracheal intratracheal instillation of lipopolysaccharide (LPS), and the other group served as blank control group . The levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) in bronchoalveolar lavage fluid (BALF) after 8, 12, 24, 36, 48, 72, 96, Pathological changes of lung tissue, percentage of polymorphonuclear leukocyte (PMN) and protein concentration in BALF of model group and blank group at 12h. RESULTS: After modeling, the concentrations of TNF-α and IL-6 in BALF were significantly increased with time and reached the peak at 24 h (P <0.01). The pathological changes of lung tissue were gradually aggravated. At 12 h, significant Alveolar damage, pulmonary edema and inflammatory cell infiltration. The percentage of PMN and the protein concentration in BALF in 12-hour model group were significantly higher than those in blank control group (P <0.01). CONCLUSIONS: Under this experimental condition, LPS 8 mg / kg can be injected into the trachea 12 h later to establish the ALI model. The ALI model can be established by detecting the concentration of TNF-α and IL-6 in BALF and the degree of lung lesions Model evaluation.