Feddersen C O, Mathias M, Murphy R C, Reeves J T, Voelkel N F
Prostaglandins. 1983 Dec;26(6):869-83. doi: 10.1016/0090-6980(83)90150-8.
Leukotriene E4 (LTE4) appears to be a rather stable product of the lipoxygenase pathway. Its action in the pulmonary circulation is unknown. Therefore we investigated its effect on the circulation of isolated rat lungs perfused with a cell- and plasma-free solution. Synthetic LTE4 in doses from .15 micrograms to 5 micrograms/.25 ml .9% NaCl injected as a bolus in the pulmonary artery during normoxia caused a fast, transient perfusion pressure increase within seconds. This was followed by a slow rise in baseline perfusion pressure (normoxia) over 25 min. In addition, 5 micrograms LTE4 caused edematogenic lung damage. Injection of 1.5 micrograms LTE4 during hypoxic vasoconstriction caused fast, transient pressure rises, similar to normoxic conditions. 6-keto-PGF1 alpha and TXB2 were measured in the lung effluent before and after LTE4 injection. Neither 6-keto-PGF1 alpha nor TXB2 production changed after LTE4 injection. Meclofenamate (.5 micrograms/ml) increased the fast, transient and the slow, sustained pressure rise. We conclude that LTE4 caused direct pulmonary vasoconstriction unrelated to cyclooxygenase products.
白三烯E4（LTE4）似乎是脂氧合酶途径的一种相当稳定的产物。其在肺循环中的作用尚不清楚。因此，我们研究了它对用无细胞和无血浆溶液灌注的离体大鼠肺循环的影响。在常氧条件下，以剂量从0.15微克到5微克/0.25毫升0.9%氯化钠的合成LTE4作为团注注入肺动脉，数秒内引起快速、短暂的灌注压升高。随后，基线灌注压（常氧）在25分钟内缓慢上升。此外，5微克LTE4导致产生水肿的肺损伤。在低氧性血管收缩期间注射1.5微克LTE4引起快速、短暂的压力升高，类似于常氧条件。在LTE4注射前后测量肺流出物中的6-酮-前列腺素F1α（6-keto-PGF1α）和血栓素B2（TXB2）。LTE4注射后，6-keto-PGF1α和TXB2的产生均未改变。甲氯芬那酸（0.5微克/毫升）增加了快速、短暂以及缓慢、持续的压力升高。我们得出结论，LTE4引起与环氧化酶产物无关的直接肺血管收缩。
