The inactivation of prostaglandin E2 is decreased by dipyridamole and sulfinpyrazone in isolated rat lungs.
The inactivation of prostaglandin E2 (PGE2) was decreased in the pulmonary circulation of isolated rat lungs, when either dipyridamole or sulfinpyrazone was infused into the pulmonary artery at the concentration of 20 microM. After pulmonary injection of 7.1 nmoles of 14C-PGE2 the amount of 15-oxo-metabolites of PGE2 in the effluent was 3.91 +/- 0.19 nmoles from control lungs and 2.05 +/- 0.19 nmoles (2P less than 0.001) in that from 20 microM dipyridamole treated lungs. The corresponding values for control and 20 microM sulfinpyrazone lungs were 4.11 +/- 0.25 and 3.03 +/- 0.14 nmoles (2P less than 0.01), respectively. The amounts of unmetabolized PGE2 were correspondingly increased in the effluents from dipyridamole and sulfinpyrazone (20 microM) lungs. Neither dipyridamole nor sulfinpyrazone had at concentration of 2 microM any significant effect on the amount of 15-oxo-metabolites in the effluent, although the amount of unmetabolized PGE2 was slightly increased in 2 microM sulfinpyrazone experiments.
D000818:Animals; D015232:Dinoprostone / Q000031:analogs & derivatives*; D004176:Dipyridamole / Q000494:pharmacology*; D008168:Lung / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D010477:Perfusion; D011458:Prostaglandins E / Q000378:metabolism*; D051381:Rats; D013442:Sulfinpyrazone / Q000494:pharmacology*
D011458:Prostaglandins E; C026346:15-ketoprostaglandin E2; D004176:Dipyridamole; D015232:Dinoprostone; D013442:Sulfinpyrazone