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目的 探讨肺动脉内皮细胞在缺氧性肺动脉高压和肺水肿发生机制中的作用。 方法 利用离体培养的猪肺动脉内皮细胞 (PAEC)为实验模型 ,通过放免分析方法检测了缺氧过程中PAEC分泌到培养液中的收缩因子内皮素 (ET- 1)及舒张因子前列环素 (PGI2 )的变化。 结果 在缺氧过程中 ,PAEC分泌 ET- 1的水平与对照组比较均明显增加 (P<0 .0 5 ) ;PAEC分泌 PGI2 的水平在缺氧开始 (12 h)时出现一过性的增加 ,但随缺氧时间的延长 (2 4h) ,PGI2 含量明显降低 (P<0 .0 5 )。 结论 缺氧过程中 PAEC分泌功能的变化可能导致肺血管收缩 ,形成缺氧性肺动脉高压 ,以及血管完整性的破坏和通透性的增加 ,形成缺氧性肺水肿。
Objective To investigate the role of pulmonary artery endothelial cells in the pathogenesis of hypoxic pulmonary hypertension and pulmonary edema. Methods The cultured porcine pulmonary artery endothelial cells (PAECs) were used as experimental models. The levels of endothelin-1 (ET-1) and prostacyclin, a relaxing factor secreted by PAEC, into culture medium during hypoxia were detected by radioimmunoassay PGI2) changes. Results During hypoxia, the level of ET-1 secreted by PAEC significantly increased compared with the control group (P <0.05). The level of PGI2 secreted by PAEC increased transiently at the beginning of hypoxia (12 h) , But PGI2 content decreased significantly with hypoxia time (24 h) (P <0.05). Conclusions The changes of PAEC secretion during hypoxia may lead to pulmonary vasoconstriction, hypoxic pulmonary hypertension, destruction of vascular integrity and increase of permeability, forming hypoxic pulmonary edema.