Pulmonary vascular responses to prostaglandins.

Pulmonary vascular responses to the endoperoxide PGH2, an endoperoxide analog, primary prostaglandins (PGE2, PGF2 alpha, and PGD2), arachidonic acid, and PGI2 were compared in the intact chest of the cat and dog. The primary prostaglandins as well as PGH2 and a stable endoperoxide analog all increase lobar arterial pressure in the dog and cat when injected into the lobar artery. Since pulmonary blood flow was held constant with a pump and left atrial pressure was unchanged, the increases in lobar arterial pressure indicate an increase in pulmonary vascular resistance. The endoperoxide analog and PGF2 alpha were very potent pressor agents in the pulmonary vascular bed. The primary prostaglandins and the endoperoxide analog had significant contractile activity in isolated segments of bovine intrapulmonary artery and vein and in canine intrapulmonary vein. The endoperoxide analog. PGF2 alpha, PGD2, and arachidonic acid, in addition to increasing pulmonary vascular resistance, increased bronchomotor tone. In contrast to the effects of the primary prostaglandins and the endoperoxide analog, PGI2 had vasodilator activity in the pulmonary vascular bed and this activity was enhanced when pulmonary vascular tone was elevated. The prostaglandin precursor arachidonic acid produced both increases and decreases in pulmonary vascular resistance, depending on dose and rate of administration, and these responses were blocked by indomethacin. These data indicate that the prostaglandins have marked but diverse activity in the pulmonary vascular bed.