CONTRIBUTION OF PROSTAGLANDINS TO THE REGULATION OF PULMONARY VASCULAR-RESISTANCE IN ADULT CATS AND DOGS

In order to determine the role of prostaglandins in the regulation of pulmonary vascular resistance, we investigated effects of prostaglandin cyclooxygenase inhibition by indomethacin (2 mg/kg), meclofenamate (2 mg/kg), and aspirin (40 mg/kg) upon canine and feline pulmonary vasoconstriction caused by two stimuli: acute hypoxia (6% 02) and exogenous PGF2α. Measurements were made utilizing an open chest, pump-perfused, in situ lung preparation. Cat pulmonary vasculatures were more responsive to hypoxia and PGF2α than were dog's. In dogs, indomethacin, meclofenamate, and aspirin all increased pulmonary vascular resistance and augmented pulmonary vasoconstrictor responses to hypoxia and PGF2α.Neither indomethacin, meclofenamate, nor aspirin affected baseline pulmonary vascular resistance of cats. Aspirin and indomethacin augmented pulmonary vasoconstriction in the cat. Meclofenamate was without effect. Further, although aspirin and indomethacin strongly inhibited pulmonary vascular pressor responses to exogenous arachidonic acid, declofenamate decreased pulmonary responses to arachidonic acid very little. All three inhibitors nearly abolished systemic responses to arachidonic acid in the cat. Exogenous PGI2 infusion decreased pulmonary vascular resistance in the cat. Prostaglandin cyclo-oxygenase activity produces a vasodilator influence, probably PGI2, in the canine pulmonary vasculature that may be significant in protecting the animal from pulmonary hypertension and its consequences. The role of the prostaglandin system in the feline pulmonary vasculature appears to be qualitatively similar, but quantitatively less, than in the dog. © 1979.