PBEF在体外循环术后肺血管内皮通透性中的机制研究

目的:探讨PBEF在体外循环术后肺血管内皮通透性增加中的机制,为提出更好的体外循环期间肺保护措施提供依据。方法:建立动物模型并进行分组,A组仅行病毒转染;B组仅行30min深低温停循环;C组行病毒转染后,再行30min深低温停循环。应用Western blot检测各组大鼠肺组织。结果:C组的PBEF、磷酸化P38MAPK、磷酸化ERK、磷酸化MLC、磷酸化VE-cadherin、磷酸化FAK表达明显高于A、B组和对照组。结论:PBEF通过P38MAPK、ERK等途径改变内皮细胞和平滑肌细胞中MLC的磷酸化状态,VE-cadherin和FAK也参与了肺血管内皮通透性增加的过程。

Research of the mechanism of PBEF in pulmonary vascular endothelial permeability increasing after CPB

Objective To investigate the mechanism of PBEF in pulmonary vascular endothelial permeability increasing after CPB,in order to provide the basis for a better lung protective measures during cardiopulmonary bypass. Method Animal models were established,group A： the rats were transfected with the lentiviral AD- PBEFshRNA; group B： the rats were took 30 min deep hypothermic circulatory arrest; group C： the rats were took 30 min deep hypothermic circulatory arrest,then transfected with the lentiviral AD-PBEFshRNA. Lung tissue was detected with Western blot. Results PBEF,phosphorylation of P38 MAPK,ERK,MLC,VE- cadherin,FAK in group C had significant difference with group A,B and the control group. Conclusion PBEF can change the phosphorylation state of the MLC in endothelial cells and smooth muscle cellsby P38 MAPK,ERK pathway. VE- cadherin and FAK also involve in the process of pulmonary endothelial permeability increasing.