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目的和方法 :研究肺动脉内皮细胞 (PAEC)在低氧性肺水肿 (HPE)发生中的作用机制 ,采用PAEC体外培养的方法 ,观察了PAEC生长状态和特征性蛋白因子Ⅷ相关抗原 (ⅧR :Ag)的变化 ,并利用PAEC融合单层通透性模型研究了低氧对PAEC融合单层的通透性的影响。结果 :PAEC生长数量无明显变化 ,但细胞的生长质量下降 ,ⅧR :Ag阳性细胞数明显下降 ,PAEC通透性明显增加 ,CaM阻断剂TFP只能部分抑制这种通透性增加。说明PAEC单层通透性的增加 ,除细胞自身骨架收缩外 ,主要是PAEC生长状态变化引起的。结论 :PAEC通透性增加是HPE的一个重要因素。
PURPOSE AND METHODS: To investigate the mechanism of pulmonary arterial endothelial cells (PAEC) in the pathogenesis of hypoxic pulmonary edema (HPE) and to investigate the effect of PAEC on the growth of PAEC and the expression of characteristic factor Ⅷ (ⅧR: Ag ), And the effect of hypoxia on the permeability of PAEC monolayer was studied by PAEC monolayer permeability model. RESULTS: There was no significant change in the number of PAECs but the quality of cells decreased. The number of ⅧR: Ag positive cells decreased obviously and the permeability of PAEC increased obviously. The CaM inhibitor TFP only partially inhibited the increase of permeability. PAEC monolayer permeability increase, in addition to the contraction of the cell’s own skeleton, the main PAEC growth status changes caused. Conclusion: Increased permeability of PAEC is an important factor in HPE.