The pulmonary vasoconstrictor response to hypoxia: effects of inhibitors of prostaglandin biosynthesis.
The main purpose of the present work was to determine whether prostaglandins (PGs) synthetised in the lungs mediate the vasoconstrictor response to acute alveolar hypoxia. Isolated and ventilated lungs of rats were perfused at 37 degrees C with homologous blood at constant-volume, pulsatile inflow, and pressor responses to 3 min periods of standardized ventilation hypoxia recorded. Indomethacin, sodium meclofenamate and acetylsalicylic acid (all 100 mug/ml), which are potent inhibitors of PG biosynthesis, did not reduce the hypoxic vasoconstrictor response. Sometimes they even enhanced this response. We conclude that PGs do not mediate the hypoxia-induced vasoconstriction. We suggest that vasodilatory PGs might act to reduce and modify pulmonary arterial hypertension due to hypoxia.
D000818:Animals; D001241:Aspirin / Q000494:pharmacology*; D001794:Blood Pressure / Q000187:drug effects; D003864:Depression, Chemical; D000860:Hypoxia; D007213:Indomethacin / Q000494:pharmacology*; D008469:Meclofenamic Acid / Q000494:pharmacology*; D011453:Prostaglandins / Q000096:biosynthesis*; D011651:Pulmonary Artery / Q000187:drug effects; D011652:Pulmonary Circulation / Q000187:drug effects*; D011667:Pulmonary Veins / Q000187:drug effects; D051381:Rats; D013268:Stimulation, Chemical; D014655:Vascular Resistance / Q000187:drug effects*; D062367:ortho-Aminobenzoates / Q000494:pharmacology*
D011453:Prostaglandins; D062367:ortho-Aminobenzoates; D008469:Meclofenamic Acid; D001241:Aspirin; D007213:Indomethacin