CYCLOOXYGENASE PRODUCTS AND CYCLIC-NUCLEOTIDE LEVELS WITH INFUSION OF ARACHIDONIC-ACID, PGI2, PGE2, PGF2, AND 6-KETO-PGF1 IN AN ISOLATED DOG LUNG

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Abstract
Arachidonic acid (AA) was infused into the pulmonary artery of an isolated dog lung perfused with a physiological salt solution. This led to elevations in pulmonary cAMP and prostaglandins (PG), including PGE2, PGF2.alpha., TXB2 (a metabolite of TXA2), and 6-keto-PGF1.alpha. (a metabolite of PGI2). The elevations were prevented by PG synthesis inhibitors. A dose of PGI2 comparable to that produced from AA led to elevations in cAMP. These elevations were not reduced by PG synthesis inhibitors; this indicated that the inhibitors did not reduce cAMP except by inhibiting metabolism of AA. The PGE2 led to lesser elevations in cAMP than did PGI2; PGF2.alpha. and 6-keto-PGF1.alpha. did not increase cAMP. Levels of cAMP were not elevated. Some of the elevation in cAMP from AA was most likely from production of PG since elevations in both were prevented by the inhibitors. AA metabolites other than PG may have also contributed to elevations in cAMP. PGI2 most likely accounted for some of the cAMP elevation from AA since PGI2 could be readily produced in amounts that elevate cAMP. The possibility remains that PGE2, the less consistent cAMP stimulators (i.e., PGF2.alpha. and 6-keto-PGF1.alpha.), TXA2, TXB or PG not measured in this study also contributed to the elevations in cAMP from AA.