Hypoxia stimulates prostacyclin synthesis by neonatal lungs.
Inhibition of prostaglandin cyclooxygenase augments hypoxic pulmonary vasoconstriction. We used a neonatal lamb lung preparation perfused with Krebs' bicarbonate buffer to characterize and quantify prostanoids produced by the pulmonary vasculature from endogenous arachidonic acid in the absence of formed blood elements during ventilation with normoxic and hypoxic gas mixtures. Prostaglandin (PG) I2 synthesis increased from 6.4 +/- 2.7 ng/min (SEM) during normoxic ventilation to 14.3 +/- 5.4 ng/min during hypoxia and returned to 4.7 +/- 1.2 ng/min with resumption of normoxia. These data demonstrate that hypoxia stimulates pulmonary vascular synthesis of prostaglandin I2 from endogenous substrate in neonatal lambs and suggest that the augmentation of hypoxic pulmonary vasoconstriction by prostaglandin cyclooxygenase inhibition is due, at least in part, to interference with the synthesis of this vasodilator prostanoid.
D000818:Animals; D000831:Animals, Newborn / Q000378:metabolism*; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000378:metabolism; D016861:Cyclooxygenase Inhibitors; D011464:Epoprostenol / Q000096:biosynthesis*; D000860:Hypoxia / Q000378:metabolism*; D008168:Lung / Q000098:blood supply / Q000378:metabolism*; D010477:Perfusion; D010812:Physical Stimulation; D011667:Pulmonary Veins / Q000378:metabolism; D012756:Sheep; D014661:Vasoconstriction
D001095:Arachidonic Acids; D016861:Cyclooxygenase Inhibitors; D016718:Arachidonic Acid; D011464:Epoprostenol