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• W2000608802 abstract "In 35 isolated dog lung preparations, the pulmonary circulation of the right lung was completely separated from that of the left so that 1 lung of each preparation could serve as a control. The lungs were ventilated with 14% O2, 6% CO2 and 80% N2 and the pulmonary circulations were perfused with a dextran-salt-bicarbonate solution containing theophylline. Samples of perfusate were assayed for cyclic AMP and cyclic GMP (radioimmunoassay). Infusions of arachidonic acid (n=6) and PGI2 (n=4) but not 6-keto-PGF1α (n=3) into the pulmonary circulation led to increases in cyclic AMP compared to control. Cyclic GMP levels were unchanged by the various infusions. Indomethacin (n=4) and acetylsalicylic acid (n=4) (prostaglandin (PG) synthesis inhibitors), and tranylcypromine (n=4) (a PGI2 synthetase inhibitor), prevented the cyclic AMP increases from arachidonic acid. This prevention was not the result of interference with the ability of cells to produce or release cyclic AMP since indomethacin (n=3), acetylsalicylic acid (n=3), and tranylcypromine (n=4) did not prevent cyclic AMP increases from PGI2. We conclude that infusion of arachidonic acid into the canine lung elevated pulmonary cyclic AMP but not cyclic GMP; that part or all of this increase most likely resulted from conversion of arachidonic acid to products of PG synthesis, particularly PGI2; that infusion of PGI2 mimicked arachidonic acid in that pulmonary cyclic AMP but not cyclic GMP was elevated, and that 6-keto-PGF1α, a metabolite of PGI2, is unlikely to account for the cyclic AMP increases in this study." @default.
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• W2000608802 date "1982-09-01" @default.
• W2000608802 modified "2023-09-27" @default.
• W2000608802 title "The effects of arachidonic acid, PGI2, and 6-keto-PGF1α on cylic nucleotide concentrations in a ventilated and artificially perfused isolated dog lung" @default.
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• W2000608802 doi "https://doi.org/10.1016/s0262-1746(82)80013-9" @default.
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