Katz S A, Halushka P V, Wise W C, Cook J A
Circ Shock. 1987;22(3):221-30.
Intravenous injection of oleic acid (OA) induces acute, edematous lung injury resembling some of the features of adult respiratory distress syndrome. One class of inflammatory agents speculated to be mediators of acute lung injury are eicosanoids. We tested the hypothesis that 5-lipoxygenase and cyclooxygenase metabolites of arachidonic acid mediate the pulmonary injury induced by OA. OA (0.1 ml), injected as a bolus into the pulmonary artery (PA) of isolated, Krebs-perfused rabbit lungs, resulted in significant (P less than .05) increases in lung weight (an index of pulmonary edema), maximum airway pressure, perfusate immunoreactive (i) 6-keto PGF1a, and a significant, though minimal, increase in perfusate i-thromboxane B2. No measurable increases were recorded in PA pressure or perfusate i-leukotriene (LT) C4/D4. Neither pretreatment with the LTD4/E4 antagonist, LY171883 (10 microM), nor the 5-lipoxygenase/cyclooxygenase inhibitor, BW755C (100 microM), attenuated the pulmonary edema. However, BW755C abrogated the increase in i6-keto PGF1a. Additionally, administration of exogenous LTD4 (100 nM) into the perfusate produced only a minimal increase in lung weight in the isolated rabbit lungs (n = 4). These results demonstrate that 5-lipoxygenase and cyclooxygenase metabolites do not appear to mediate OA-induced injury in the isolated, Krebs-perfused rabbit lung.
静脉注射油酸（OA）可诱发急性、水肿性肺损伤，其某些特征类似于成人呼吸窘迫综合征。一类被推测为急性肺损伤介质的炎症因子是类花生酸。我们检验了以下假设：花生四烯酸的5-脂氧合酶和环氧化酶代谢产物介导了OA所致的肺损伤。将OA（0.1 ml）一次性注入离体的、用Krebs液灌注的兔肺肺动脉（PA）中，导致肺重量（肺水肿指标）、最大气道压力、灌流液免疫反应性（i）6-酮-前列腺素F1α显著（P<0.05）增加，灌流液i-血栓素B2虽有显著增加但增幅极小。肺动脉压力或灌流液i-白三烯（LT）C4/D4未见可测量的增加。用白三烯D4/白三烯E4拮抗剂LY171883（10 μM）或5-脂氧合酶/环氧化酶抑制剂BW755C（100 μM）预处理均未减轻肺水肿。然而，BW755C消除了i-6-酮-前列腺素F1α的增加。此外，向灌流液中加入外源性白三烯D4（100 nM）仅使离体兔肺的肺重量有极小增加（n = 4）。这些结果表明，在离体的、用Krebs液灌注的兔肺中，5-脂氧合酶和环氧化酶代谢产物似乎并未介导OA所致的损伤。
