Dipyridamole interferes with the incorporation of arachidonic acid and stimulates prostacyclin production in rat lungs.
Following the injection of 4 nmol of 14C-arachidonic acid into the pulmonary circulation of rat isolated lungs more than 90% of the radioactivity was retained by the lung tissue. When dipyridamole (20 microM) was infused into the pulmonary circulation during 14C-arachidonate injection the amount of radiolabel was increased in diacylglycerols as well as in phosphatidylinositol and phosphatidylserine of the perfused lungs whereas the amount of radioactivity was decreased in phosphatidylethanolamine. When dipyridamole was infused into the lungs prelabelled with 14C-arachidonic acid the distribution of radiolabel in different lung lipid fractions was not changed significantly. However, dipyridamole seemed to stimulate the formation of prostacyclin in rat lungs as the amount of 6-keto-PGF1 alpha was increased in the perfusion effluent. The present study indicates that dipyridamole interferes with the incorporation of arachidonic acid into different lipids in rat lungs. In addition, the release of prostacyclin seems to be stimulated by dipyridamole.
D015121:6-Ketoprostaglandin F1 alpha / Q000032:analysis; D000818:Animals; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000378:metabolism*; D004176:Dipyridamole / Q000494:pharmacology*; D011464:Epoprostenol / Q000096:biosynthesis*; D008055:Lipids / Q000032:analysis; D008168:Lung / Q000378:metabolism*; D008297:Male; D011863:Radioimmunoassay; D051381:Rats; D011919:Rats, Inbred Strains
D001095:Arachidonic Acids; D008055:Lipids; D016718:Arachidonic Acid; D015121:6-Ketoprostaglandin F1 alpha; D004176:Dipyridamole; D011464:Epoprostenol