摘要
目的探讨机械通气对大鼠肺组织中CC10蛋白表达的影响及CC10对肺炎症反应的影响。方法建立不同潮气量机械通气大鼠动物模型,分为对照组、小潮气量组和大潮气量组。通气4 h后采用Western blot法测定肺组织CC10蛋白含量,计算细支气管上皮Clara细胞百分率;酶联免疫吸附法测定肺组织匀浆中TNF-α,MIP-2含量,对肺泡灌洗液行中性粒细胞计数。结果与对照组和小潮气量组相比,大潮气量组肺组织CC10表达降低,TNF-α、MIP-2升高,细支气管上皮Clara细胞百分率降低,差异均有统计学意义(P均<0.05);与对照组相比,小潮气量组上述指标无明显变化,差异无统计学意义(P>0.05)。结论大潮气量机械通气引起肺组织中抗炎因子CC10表达减少,炎症因子TNF-α、MIP-2表达增加,肺损伤加重。
Objective To investigate the effects of mechanical ventilation on CC10 protein levels in hmg tissues of rats and the effects of CC10 on lung inflammation reactions. Methods Thirty normal Wistar rats weighing 200-250 g were randomly divided into 3 groups （ 10 in each） ： the control group, the low tidal vohane group （tidal volume VT = 8 ml/kg, ventilation time t = 4 h）, and the high tidal volume group （VT = 40 ml/kg, t = 4 h）. After ventilation, the rats were sacrificed and the lungs were removed. Levels of CC10, TNF-a and MIP-2 were determined by ELISA. The percentage of Clara cells in the bronehiolar epithelium and PMN was determined in the broncho-alveolar lavage fluid （BALF）. Results High tidal volume ventilation induced serious histopathologieal damage in lung tissues of rats. Both TNF-α and MIP-2 in lung tissues and PMN in BALF significantly increased in the high tidal volume group as compared with the control group and the low tidal volume group （ P 〈 0.05）. The levels of CC10 in lung tissues and the percentage of Clara cells was significantly lower in the high tidal volume group than those in the control and low tidal volume groups（ P 〈 0.05）, but they were not statistically different between the control and the low tidal volume groups （ P 〉 0.5）. Conclusion High tidal volume ventilation decreases the expression of CC10 in lung tissues and increases the expressions of TNF-α, nd MIP-2, and induces heavy lung injury.
出处
《山东大学学报（医学版）》
CAS
北大核心
2008年第11期1024-1027,共4页
Journal of Shandong University:Health Sciences
