Cyclooxygenase inhibition prevents PMA-induced increases in lung vascular permeability.
Cyclooxygenase inhibition prevents PMA-induced increases in lung vascular permeability.
复制标题
环加氧酶抑制可防止 PMA 诱导的肺血管通透性增加。
DOI：
10.1152/jappl.1990.69.4.1494
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Dahms,TE
中科院分区：
文献类型：
--
作者：
Zanaboni,PB;Bradley,JD;Baudendistel,LJ;Webster,RO;Dahms,TE
在离体恒流血液灌注兔肺中研究了环氧合酶抑制对佛波醇肉豆蔻酸酯乙酸酯 (PMA) 诱导的急性肺损伤的影响。 PMA 导致肺动脉压增加 51%（通过血管闭塞压力测量，位于动脉和中段），微血管通透性增加 71%（通过微血管液体过滤系数 Kf 测量），以及灌注液血栓素 (Tx) B2 水平增加近三倍。使用三种化学性质不同的抑制剂吲哚美辛（10（-7）和10（-6）M）、甲氯芬那酯（10（-6）M）和布洛芬（10（-5）M）抑制环加氧酶，可以防止Kf增加，而不影响PMA给药后肺动脉压增加或阻力分布变化。通过用特异性Tx合酶抑制剂OKY-046预处理或输注TxA2受体拮抗剂SQ 29548来研究TxA2的具体作用；这两种化合物都未能防止 PMA 引起的渗透性或血管阻力增加。这些结果表明环加氧酶介导的花生四烯酸产物（TxA2 除外）介导 PMA 诱导的通透性增加，但不介导高血压。
The effect of cyclooxygenase inhibition in phorbol myristate acetate (PMA)-induced acute lung injury was studied in isolated constant-flow blood-perfused rabbit lungs. PMA caused a 51% increase in pulmonary arterial pressure (localized in the arterial and middle segments as measured by vascular occlusion pressures), a 71% increase in microvascular permeability (measured by the microvascular fluid filtration coefficient, Kf), and a nearly threefold increase in perfusate thromboxane (Tx) B2 levels. Cyclooxygenase inhibition with three chemically dissimilar inhibitors, indomethacin (10(-7) and 10(-6) M), meclofenamate (10(-6) M), and ibuprofen (10(-5) M), prevented the Kf increase without affecting the pulmonary arterial pressure increase or resistance distribution changes after PMA administration. The specific role of TxA2 was investigated by pretreatment with OKY-046, a specific Tx synthase inhibitor, or infusion of SQ 29548, a TxA2 receptor antagonist; both compounds failed to protect against either the PMA-induced permeability or the vascular resistance increase. These results indicate that cyclooxygenase-mediated products of arachidonic acid other than TxA2 mediate the PMA-induced permeability increase but not the hypertension.