The metabolism of arachidonic acid in isolated hamster, rat and guinea pig lungs

Abstract

The perfusion effluent from isolated rat lungs caused relaxations of superfused strips of bovine (BCA) and pig (PCA) coronary arteries. The effluent from hamster lungs had similar effect on BCA. Bolus injections of arachidonate (AA, 10–20 μg) into rat lungs caused further relaxations of superfused BCA and contractions of rat stomach strip (RSS). AA injections into guinea pig lungs resulted in dose dependent contractions of BCA and PCA. Similar dose dependent contractions of PCA and RSS were seen in hamster experiments, however the responses of BCA varied with the AA dose. Infusion of AA (5–25 μg/min) into guinea pig lungs resulted in dose dependent contractions of superfused PCA and BCA. In hamster experiments AA infusion (5 μg/min) caused a small relaxation of BCA, but had no effect on PCA. When 14 C-AA was injected into the pulmonary circulation, the amounts of metabolites were greater in the perfusion effluent from hamster than from rat lungs. In rat lungs 6-oxo-PGF 1α was one of the main metabolites. In contrast, in hamster lungs this metabolite represented only a small part of the total metabolite formation. Thromboxane B 2 was one of the main metabolites formed in hamster lungs and its rate of formation increased greatly with increasing AA doses. The results indicate that the metabolite pattern of arachidonate in isolated rat lungs is different from that in hamster and guinea pig lungs. The total rate of AA metabolism in rat lungs is smaller than in hamster lungs.