Thromboxane mediates the increase in alveolar surfactant pool induced by free fatty acid infusion in the rabbit

Abstract

Intravenous infusion of free fatty acid (FFA) produces pulmonary edema and an increase in the alveolar surfactant content of the rabbit. In order to identify a likely mediator of this lung response to FFA, we used inhibitors of cyclo-oxygenase (indomethacin, 15 mg.kg<sup>-1</sup> i.v., or meclofenamate, 5 mg.kg<sup>-1</sup> i.v.) and thromboxane syn-thetase inhibitors (imidazole, 50 mg.kg<sup>-1</sup> i.v. or dazoxiben, 2 mg.kg<sup>-1</sup> i.v.) which were administered before FFA, 20 mg. kg<sup>-1</sup> min<sup>-1</sup> i.v., in four different experimental series (n = 54). Lung surfactant was measured in bronchial-alveolar lavage fluid by determining disaturated phosphatidylcholine (DSPC). Both kinds of inhibitors blocked the increase in FFA-induced DSPC. They increased the survival rate but they only slightly changed the post-FFA morphofunctional pulmonary alterations. We conclude that the increase in alveolar surfactant induced by FFA is likely mediated by thromboxane. This mediator