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Original Article

Cyclooxygenase Metabolites Contribute to Oleic Acid-induced Lung Edema by a Pressure Effect

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Pages 69-82 | Received 06 May 1986, Accepted 28 Sep 1986, Published online: 02 Jul 2009
 

Abstract

We investigated the role that lung-derived arachidonic acid metabolites play in the acute changes in pulmonary hemodynamics, airway function, and lung fluid balance following oleic acid-induced injury in the isolated blood free perfused lung. A bolus injection of oleic acid (OA) emulsion (12 mg) into the pulmonary artery caused a rapid increase in pulmonary arterial pressure, inspiratory pressure, and weight gain. These pathophysiologic changes were not due to emboli per se, but were correlated with release of the vaso- and broncho-constrictive prostanoids, tbromboxane A2 (measured as throm-boxane B2) and prostaglandin F2α. The leukotrienes (C4, D4, and E4) and prostacyclin (measured as 6 keto-prostaglandin F1α) were not released by OA injury. Ibuprofen, a cyclooxygenase inhibitor, blocked the release of the vasoconstrictive prostanoids and also attenuated the rise in pressures and the development of edema indicating an important functional role for the prostanoids in the fluid imbalance. Ibuprofen also attenuated the increase in bronchoalveolar lavage protein but the protein leak was not completely prevented, suggesting that OA-induced increases in protein permeability occurred independently of prostanoid or leukotriene action. These data indicate that OA-induced edema formation was greatly amplified by arachidonic acid mediated pressure increases.

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