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目的 主要探讨一氧化氮（ＮＯ） 和诱导型一氧化氮合酶（ｉＮＯＳ）在内毒素（ＬＰＳ） 诱导的大鼠急性肺损伤（ＡＬＩ）的作用机制及大黄对其影响。方法 在雄性Ｗｉｓｔａｒ 大鼠利用舌下静脉注射ＬＰＳ复制ＡＬＩ动物模型，动物分为４ 组：ＬＰＳ组、对照组、大黄治疗组、地塞米松组。观察大体标本，组织病理以及生物学标志：肺湿／干重比、肺泡灌洗液中性粒细胞比、蛋白含量、肺血管通透性和肺泡通透性指数。同时测定血浆ＮＯ和肺组织匀浆ｉＮＯＳ活性。结果 ＬＰＳ组与对照组相比，肺组织病理显示肺间质及肺泡明显损伤和细胞浸润。其生物学标志均显著升高（Ｐ＜０－０１），ＮＯ 和ｉＮＯＳ也显著升高（ Ｐ＜０－０１） ，地塞米松和大黄干预治疗组则表现组织病理明显减轻。上述肺损伤生物标记物及ＮＯ、ｉＮＯＳ也相应下降（ Ｐ＜ ０－０５） 。结论 在ＬＰＳ诱导的ＡＬＩ大鼠动物模型中证明ＮＯ和ｉＮＯＳ在ＡＬＩ的发病过程中起到较为关键性的作用，用地塞米松、大黄进行干预治疗，可使损伤减轻相应地也使ＮＯ、ｉＮＯＳ浓度下降，表明这２ 种药物对ＬＰＳ诱导的ＡＬＩ具有保护作用，其机制可能是通过抑制ＮＯ和ｉＮＯＳ活性实现。
Objective To investigate the mechanism of nitric oxide (NO) and inducible nitric oxide synthase (iNOS) induced by endotoxin (LPS) in rats with acute lung injury (ALI) and the effect of rhubarb on it. Methods The animal models of ALI were established by sublingual intravenous injection of LPS in male Wistar rats. The animals were divided into 4 groups: LPS group, control group, rhubarb treatment group and dexamethasone group. Gross specimens, histopathology and biological markers were observed: lung wet / dry weight ratio, neutrophilic ratio of alveolar lavage fluid, protein content, pulmonary vascular permeability and alveolar permeability index. Plasma NO and lung homogenate iNOS activity were measured simultaneously. Results Compared with the control group, the lung histopathology showed obvious damage and cell infiltration of lung interstitium and alveoli in LPS group. The biomarkers were significantly increased (P <0-01), NO and iNOS were also significantly increased (P <0-01), dexamethasone and rhubarb intervention group showed a significant reduction in histopathology. The lung injury biomarkers and NO, iNOS also decreased accordingly (P <0-05). Conclusion NO and iNOS play a key role in the pathogenesis of ALI in LPS-induced ALI rat model. Intervention treatment with dexamethasone and rhubarb can reduce the damage and accordingly make NO, iNOS concentration Decreased, indicating that these two drugs have a protective effect on LPS-induced ALI, the mechanism may be through the inhibition of NO and iNOS activity.