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目的 :观察肺血管内皮细胞受损在大鼠急性肺损伤发病中的作用及地塞米松的影响。方法 :给Wistar大鼠静脉注射脂多糖 (LPS 5mg/kgBW)复制急性肺损伤模型。采用ELISA、放射免疫、原位杂交等多种方法测定肺组织ICAM - 1mRNA表达、iNOS活性、血中TNF -α、NO-2 /NO3-、ACE含量及肺血管通透性、肺泡灌洗液中细胞数、蛋白含量等的变化。结果 :注射LPS后 ,肺血管ICAM - 1mRNA表达增加 ,从 1h开始至 2 4h达高峰。肺组织匀浆iNOS活性升高、肺血管通透性升高、肺泡灌洗液中中性粒细胞数量增加 ,巨噬细胞数量减少、蛋白含量增加 ,血中TNF -α、NO2 -/NO3-含量升高而ACE含量下降等变化多在注LPS后 2h明显。预先给予地塞米松对上述多种指标的变化有明显缓解作用。结论 :提示LPS通过损伤肺血管内皮细胞导致急性肺损伤 ,地塞米松对其有一定保护作用
Objective: To observe the role of pulmonary vascular endothelial cell damage in the pathogenesis of acute lung injury in rats and the effect of dexamethasone. Methods: Acute lung injury was induced by lipopolysaccharide (LPS 5 mg / kg BW) intravenously in Wistar rats. The expression of ICAM - 1mRNA, iNOS activity, the levels of TNF - α, NO - 2 / NO3- and ACE in the lung tissue and pulmonary vascular permeability were measured by ELISA, radioimmunoassay and in situ hybridization. In the cell number, protein content and other changes. Results: After injection of LPS, the expression of ICAM - 1 mRNA in pulmonary arteries increased from 1h to 24h. The lung tissue homogenate iNOS activity increased, pulmonary vascular permeability increased, the number of alveolar lavage fluid neutrophils increased, the number of macrophages decreased, increased protein content, blood levels of TNF-α, NO2 - / NO3- Changes in the content of ACE and declines in more than 2h after injection of LPS obvious. Pre-given dexamethasone on the changes in a variety of indicators significantly alleviate the role. Conclusion: It is suggested that LPS can induce acute lung injury by injuring pulmonary vascular endothelial cells, and dexamethasone may have some protective effects