Respiratory effects of lipopolysaccharide-induced inflammatory lung injury in mice
Respiratory effects of lipopolysaccharide-induced inflammatory lung injury in mice
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DOI：
10.1034/j.1399-3003.2000.15a16.x
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发表时间：
2000-01-01
影响因子：
24.3
通讯作者：
Zin, WA
中科院分区：
文献类型：
--
作者：
Faffe, DS;Seidl, VR;Zin, WA
脂多糖（LPS）引起的肺损伤的致病机制尚未分类。本研究检查了小鼠吸入内毒素后的生理变化，并将其与肺部炎症特征相关。在吸入盐水或大肠杆菌LPS（0.3（L0.3）或10 mg.mL（-1）后，在不同时间（3、24、48和72小时）对BALB/c小鼠的肺力学、组织病理学和支气管肺泡灌洗液（BALF）进行分析(L10))，对小鼠进行镇静、麻醉和通气。胸壁切除后静态（Est）和动态（E-dyn）弹性、Delta E（E-dyn-E-st）、阻力（Delta P-1）和粘弹性/不均匀压力（Delta P-2）以及Delta P-1+Delta P-2（Delta P-tot）通过充气末期闭塞法获得。准备肺进行组织病理学检查。在平行组中，评估 BALF 中的肿瘤坏死因子 (TNF)-α、中性粒细胞和蛋白质。L0.3 和 L10 显示在大量中性粒细胞浸润之前 TNP-α 的时间依赖性产生。在 L10 BALF 中，蛋白质水平在 24 小时和 48 小时增加，Est 和 Edyn 在 L0.3 早期增加（65%、63%）和 L10（41%、51%）。 L10中Delta E、Delta P-2和Delta P-tot呈现逐渐上升趋势。 72 小时时，所有组均相似。 L0.3显示细胞结构早期增加，在72小时恢复正常，L10呈现相同的模式，细胞计数保持升高直到72小时。总之，吸入脂多糖导致小鼠肺部弹性和粘弹性变化，以及肿瘤坏死因子-α产生和中性粒细胞浸润。
The pathogenic mechanisms of lipopolysaccharide (LPS)-induced lung injury have not been classified. This study examined the physiological changes after endotoxin inhalation and related those to features of pulmonary inflammation in mice.Pulmonary mechanics, histopathology, and bronchoalveolar lavage fluid (BALF) from BALB/c mice were analysed at different occasions (3, 24, 48 and 72 h) after inhalation of saline or LPS from Excherichia coli (0.3 (L0.3) or 10 mg.mL(-1) (L10)), Mice were sedated, anaesthetized, and ventilated. After chest wall resection static (Est) and dynamic (E-dyn) elastances, Delta E (E-dyn-E-st), resistive (Delta P-1) and viscoelastic/ inhomogeneous pressures (Delta P-2), and Delta P-1+Delta P-2 (Delta P-tot) were obtained by end-inflation occlusion method. Lungs were prepared for histopathology, In parallel groups, tumour necrosis factor (TNF)-alpha, neutrophils, and protein were evaluated in the BALF.L0.3 and L10 showed a time-dependent production of TNP-alpha preceding a massive neutrophil infiltration. In L10 BALF there was an increase in protein level at 24 and 48 h, Est and Edyn increased early in L0.3 (65%, 63%) and L10 (41%, 51%). In L10 Delta E, Delta P-2 and Delta P-tot 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.