抽象的
脂多糖(LPS)诱导的肺损伤的致病机制尚未被分类。本研究检测了内毒素吸入后的生理变化,并将其与小鼠肺炎的特征相关。在从大肠杆菌吸入盐水或LPS后,在不同的场合(3,24,48和72h)分析来自BALB / C小鼠的肺部力学,组织病理学和支气管肺泡灌洗液(3,24,48和72小时)(0.3(l0.3)或10Mg x ml(-1)(l10))。小鼠镇静,麻醉,通风。胸壁切除静态(EST)和动态(EDYN)弹性,通过最终膨胀闭塞方法获得δ(EDYN-EST),电阻(Deltap1)和粘弹性/不均匀压力(Deltap2)和Deltap1 + Deltap2(Deltaptot)。为组织病理学制备肺部。在平行组中,在BALF中评估肿瘤坏死因子(TNF) - 嗜中性粒细胞和蛋白质。L0.3和L10显示出在巨大的中性粒细胞渗透之前的TNF-α的时间依赖性生产。在L10 Balf中,24和48小时的蛋白质水平增加。 Est and Edyn increased early in L0.3 (65%, 63%) and L10 (41%, 51%). In L10 deltaE, deltaP2, and deltaPtot showed a gradual rise. At 72 h all groups were similar. L0.3 showed an early increase in cellularity, which returned to normal at 72 h. L10 presented the same pattern with the cell count remaining elevated until 72 h. In conclusion, lipopolysaccharide inhalation led to elastic and viscoelastic pulmonary changes together with tumour necrosis factor-alpha production and neutrophil infiltration in mouse lung.