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作 者:洪欣[1] 尹昭云[1] 孙兴斌[1] 谢印芝[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:《中华航空航天医学杂志》1999年第4期206-208,共3页Chinese Journal of Aerospace Medicine
摘 要: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 (PAEC) in machanism of developing hypoxic pulmonary artery hypertension and pulmonary edema. Mothods The specimens of swine PAEC cultured in vitro were used as experimental models. They we randomly divided into two groups: the hypoxia group (with condition of 3%O 2,92%N 2,5%CO 2),and control group (21%O 2,74%N 2,5%CO 2).The contents of endothelin 1 (ET 1, vasoconstrictor) and prostacyclin (PGI 2, vasodilator) secreted by PAEC in the culture media were determined hy radioimmuno analysis technique 12 h and 24 h after exposure to the experimental conditions. Results The ET 1 contents of hypoxia group in media released by PAEC were significantly higher than those of control group ( P <0 05) both 12 h and 24 h after culturing in experimental condition. The PGI 2 content of hypoxia group measured 12 h after exposure was significantly higher than that of control group, but it became significantly lower than that of control group when it was measured 24 h after exposure. Conclusions It is suggested that the increase of PAEC ET 1 secretion and decrease of PGI 2 secretion may play an important role in developing hypoxia pulmonary artery hypertension. In addition, they possess negative effect on integrity of vascular wall and pulmonary edema may be resulted due to increase of permeabilily of vascular wall.
分 类 号:R852.11[医药卫生—航空、航天与航海医学]
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