The role of prostaglandins as mediators of alveolar hypoxic vasoconstriction was investigated in dogs with the use of the prostaglandin synthesis inhibitors, aspirin and indomethacin. Alveolar hypoxia was induced by inserting double-lumened endotracheal tube into the carina and ventilating one lung with nigrogen while maintaining normal systemic oxygenation with 100% O(2) ventilation to the other lung. Relative perfusion to each lung was determined with 133Xenon and external counters. Infusions up to 25 mg/kg of indomethacin and up to 250 mg/kg of aspirin did not block the shift in perfusion from the alveolar hypoxic lung. In fact, the shift in perfusion from the alveolar hypoxic lung was slightly augmented by aspirin (P = 0.03). Thus, no positive role was demonstrated in the dog for prostaglandins in producing the vasoconstriction of alveolar hypoxia.