【摘要】 通过肺动脉内皮细胞对氧自由基刺激的反应探索氧自由基对肺血管的损伤和引起肺动脉高压的机理。以黄嘌呤氧化酶作用于次黄嘌呤而产生氧自由基，观察其对体外培养小母牛肺动脉内皮细胞（CPAE）的增殖和分泌血管紧张素Ⅱ（ATⅡ）的影响。结果：揭示氧自由基不但可抑制CPAE细胞生长，可导致细胞的损伤，而且可刺激其分泌ATⅡ。在含0．1mmol/L次黄嘌呤的细胞培养液中加入0．05U/ml黄嘌呤氧化酶的相同条件下，氧自由基的上述作用与细胞接触时间呈正相关。刺激15min时，即可见CPAE分泌ATⅡ水平升高，为对照水平的2～3倍。刺激30min时，ATⅡ的分泌达高峰，而刺激60min时，ATⅡ的分泌能力反而减弱，细胞形态也发生改变，表明细胞的明显损伤。结果提示氧自由基、黄嘌呤氧化酶可能通过刺激ATⅡ的分泌而参与急性肺损伤、急性呼吸窘迫综合征（ARDS）时肺动脉高压的形成。更多还原

【Abstract】 The effects of oxygen free radical on pulmonary vascular endothelial cells and the pathogenesis of pulmonary hypertension in acute lung injury and acute respiratory distress syndrom (ARDS). The growth and secretion of angiotensin Ⅱof cultured endothelial cells of pulmonary artery of female young cow (CPAE) stimulated by hypoxanthine plus xanthine oxydase were observed. Results: Oxygen free radical induced the cell damage and inhibited the growth of CPAE, and stimulated the secretion of angiotensin Ⅱ as Well. The effects as above were dependent on exposure time to oxygen free radical at the same concentration of 0. 05U/ml of xanthine oxidase in MEME with 0.1mmol/L of hypoxanthine. In the group of 15 minutes exposing oxygen free radical, the AT Ⅱ level was 2~ 3times higher than that in the control group. The AT Ⅱ level reached to the peak when CPAE exposed to oxygen radical for 30 min. However, the AT Ⅱ content reduced When CPAE stimulated by Oxygen radical for 60 min with the highest rate of apoptosis, much more significant inhibition of cell growth and severe cell deformation. Oxygen radical, xanthine oxidase and angiotensin Ⅱ attended the pathophysiological process in ARDS.更多还原