低氧时肺动脉内皮细胞单层通透性变化  

THE CHANGE OF PULMONARY ARTERY ENDOTHELIAL CELL DURING HYPOXIA

作　　者：洪欣[1] 尹昭云[1] 孙兴斌[1] 吕永达[1] 

机构地区：[1]军事医学科学院卫生学环境医学研究所,天津300050

出　　处：《中国应用生理学杂志》2000年第1期41-44,共4页Chinese Journal of Applied Physiology

摘　　要：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。Aim and methods: To investigate the role of pulmonary artery endothelial cell(PAEC)on the mechanism of hypoxic pulmonary edema (HPE), the growth situation, the characteristic of endothelial cells (factor Ⅷ related antigen), the permeability of the monolayer PAEC were investigated during hypoxia using the PAEC cultured in vitro as a model. Results: The growth number of PAEC either in hypoxia or normoxia conditions revealed no difference during the period of 48 hour cultured( P >0. 05). The numbers of positive immunofluoescence PAEC of factor Ⅷ related antigen in PAECs of hypoxic groups were lower than those of normoxic groups. PAEC monolayer permeability of albumin was significantly enhanced in hypoxic groups compared with those in normoxic groups. The inhibitor of calmodmin, TFP only partly attenuated the enhancement of the permeability. These results indicated that, apart from the contraction of cytoskeleton protein of cells that lead to the formation of the intercellular gaps, the main reasons for the change of permeability is the growth situation of the PAEC during hypoxia. Conclusions: The change of the PAEC permeability would play an important role in the occurrence of the HPE.

关 键 词：低氧 肺动脉内皮细胞 通透性 低氧性肺水肿 

分 类 号：R563.902[医药卫生—呼吸系统] R594.302[医药卫生—内科学]