Beneficial effects of ibuprofen in oleic acid induced lung injury.
Beneficial effects of ibuprofen in oleic acid induced lung injury.
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布洛芬对油酸引起的肺损伤的有益作用。
DOI：
10.1016/0022-4804(87)90145-4
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发表时间：
1987
期刊：
影响因子：
--
通讯作者：
Halushka,PV
中科院分区：
文献类型：
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作者：
Fuhrman,TM;Hollon,MF;Reines,HD;Olanoff,LS;Halushka,PV
花生四烯酸的代谢物，特别是血栓素，被认为是肺损伤的介质。糖皮质激素类固醇可通过抑制磷脂酶 A2 或布洛芬抑制脂肪酸环加氧酶来减少血栓素 A2 的形成。本研究旨在确定布洛芬、甲泼尼龙或两者的组合是否可以改善油酸引起的肺损伤。五组狗安装了肺动脉导管和血管外肺水 (EVLW) 导管，并用 100% O2 通气。在油酸输注之前和之后进行血流动力学和肺部参数的系列测定。还测定了血浆免疫反应性血栓素 B2 (iTxB2) 和布洛芬水平。油酸迅速引起严重的肺损伤，表现为低氧血症和血管外肺水增加。仅接受油酸的对照组血浆 iTxB2 显着升高。单独输注布洛芬不会改变肺功能和血流动力学参数。布洛芬减轻了油酸引起的低氧血症并增加了 EVLW，但没有显着降低血浆 iTxB2。甲基强的松龙不能阻止血浆 iTxB2 的增加，并且在预防低氧血症和 EVLW 增加方面不如布洛芬有效。布洛芬和甲基泼尼松龙的组合确实显着抑制了 iTxB2 的产生，但与单独使用任何一种药物相比，它们组合时对低氧血症和 EVLW 增加的保护作用较小。这些结果表明，布洛芬可能对油酸诱导的肺损伤具有保护作用，这种作用不是通过抑制脂肪酸环加氧酶介导的。该结果还进一步证明血栓素可能不是油酸引起的肺损伤的致病因素。
Metabolites of arachidonic acid, particularly thromboxanes, have been implicated as mediators of lung injury. The formation of thromboxane A2can be decreased by glucocorticoid steroids by inhibiting the enzyme phospholipase A2or by ibuprofen which inhibits fatty acid cyclooxygenase. This study was performed to determine if ibuprofen, methylprednisolone, or a combination of both could improve the pulmonary injury induced by oleic acid. Five groups of dogs were instrumented with pulmonary artery and extravascular lung water (EVLW) catheters and ventilated with 100% O2. Serial determinations of hemodynamic and pulmonary parameters were performed before and after oleic acid infusion. Plasma immunoreactive thromboxane B2(iTxB2) and ibuprofen levels were also determined. Oleic acid rapidly induced a significant pulmonary injury as evidenced by hypoxemia and increases in extravascular lung water. Plasma iTxB2rose significantly in the control group receiving only oleic acid. Pulmonary function and hemodynamic parameters were not changed by ibuprofen infusion alone. Ibuprofen attenuated the oleic acid induced hypoxemia and increased EVLW but did not significantly reduce plasma iTxB2. Methylprednisolone did not prevent the increase in plasma iTxB2and was less effective than ibuprofen in preventing hypoxemia and increases in EVLW. The combination of ibuprofen and methylprednisolone did significantly inhibit the production of iTxB2, however in combination they protected less against the hypoxemia and increased EVLW than either agent alone. These results indicate that ibuprofen may have a protective effect in oleic acid induced lung injury that is not mediated through the inhibition of fatty acid cyclooxygenase. The results are also further evidence that thromboxane is probably not a pathogenetic factor in oleic acid induced lung injury.