The effects of the prostaglandin endoperoxide, PGH2, and a stable endoperoxide analog were compared on the canine pulmonary vascular bed under conditions of controlled blood flow. The analog produced dose related increases in lobar arterial and small vein pressure when injected into the perfused lobar artery. The increase in resistance in response to the analog was greater during retrograde perfusion than during forward perfusion. These data suggest that the analog increases resistance to flow by constricting pulmonary veins and upstream vessels. The increase in resistance was similar when the lung was perfused with dextran or blood and the response was not different when the lung was ventilated or collapsed. The response was not attenuated by indomethacin, an inhibitor of prostaglandin synthesis. These data suggest that the response to the analog is not related to changes in bronchomotor tone, platelet aggregation, or enhanced prostaglandin synthesis. Although the analog was a potent pressor substance, PGH2 itself produced only small increases in pulmonary vascular resistance. However, PGH2 had greater contractile activity than the analog on isolated helical segments of canine intrapulmonary vein. The present study suggests that endoperoxides may represent an active form of the prostaglandins in the lung but that their effects would be localized in the tissue in which they are formed because of their extremely short biologic half life.
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