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).