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目的 探讨细胞间粘附分子 1(ICAM - 1)在机械通气致肺损伤中的作用。方法 2 4只普通健康小猪 ,随机等分为对照组、低潮气量组 (A组 )、正常潮气量组 (B组 )及大潮气量组 (C组 )。采用持续给予小猪不同潮气量通气模型 ,利用免疫组织化学技术、酶联免疫法和髓过氧化物酶(MPO)测定法 ,分别检测不同潮气量组通气 1d、3d、7d后肺血管内皮细胞表面ICAM 1的表达量 ,血清和肺组织匀浆中肿瘤坏死因子α(TNF α)含量及MPO活性的变化。结果 A、B、C组血清、肺组织匀浆TNF α含量、MPO活性及肺血管内皮细胞表面ICAM 1表达量均较对照组升高 (P <0 .0 5或 0 .0 1) ,其中 3d后 ,TNF α达峰值 ,7d后 ,MPO活性及肺血管内皮细胞ICAM 1表达量达峰值 ,以A、C组明显。结论 ICAM 1在机械通气致肺损伤中可能发挥重要作用 ,且与TNF α的介导有关
Objective To investigate the role of intercellular adhesion molecule - 1 (ICAM - 1) in lung injury induced by mechanical ventilation. Methods 2 4 normal healthy piglets were randomly divided into control group, low tidal volume group (A group), normal tidal volume group (B group) and large tidal volume group (C group). The sustained-release piglets with different tidal volume ventilation models were used to detect the changes of pulmonary vascular endothelial cells (VECs) after 1, 3 and 7 days of ventilation with different tidal volume respectively by immunohistochemistry, enzyme-linked immunosorbent assay and myeloperoxidase (MPO) The expression of ICAM 1, the content of tumor necrosis factor α (TNF α) and the activity of MPO in serum and lung homogenate. Results The levels of TNFα, MPO and the expression of ICAM 1 on the surface of pulmonary vascular endothelial cells were significantly increased in groups A, B and C as compared with the control group (P <0.05 or 0.01) After 3 days, TNFα reached its peak. After 7 days, MPO activity and expression of ICAM 1 in pulmonary vascular endothelial cells peaked, especially in A and C groups. Conclusion ICAM 1 may play an important role in lung injury induced by mechanical ventilation and is related to the mediation of TNF α