Differential actions of the prostaglandins on the pulmonary vascular bed.
We have reported that administration of cyclooxygenase inhibitors such as indomethacin and meclofenamate results in a slow gradual increase in pulmonary vascular resistance in the intact dog (21). It has been shown that a PGI2, "like" substance is continually released by the lung (6). We have, therefore, suggested that under resting conditions, the pulmonary vascular bed is maintained in a dilated state by production of a vasodilator product in the cyclooxygenase pathway (10,21). Recent evidence suggests that this vasodilator product in the cyclooxygenase pathway is a PGI2 'like" substance (6,13,20).
D000818:Animals; D001095:Arachidonic Acids / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects; D002415:Cats; D004285:Dogs; D011464:Epoprostenol / Q000494:pharmacology*; D005260:Female; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D011449:Prostaglandin Endoperoxides / Q000494:pharmacology*; D011453:Prostaglandins / Q000494:pharmacology*; D011463:Prostaglandins H / Q000494:pharmacology*; D011652:Pulmonary Circulation / Q000187:drug effects*; D012039:Regional Blood Flow / Q000187:drug effects
D001095:Arachidonic Acids; D011449:Prostaglandin Endoperoxides; D011453:Prostaglandins; D011463:Prostaglandins H; D011464:Epoprostenol; D007213:Indomethacin