Maternal aspirin administration inhibits pulmonary arachidonic acid metabolism in fetal rabbits.
Pregnant rabbits were treated with aspirin (100 mg/kg/day) for ten consecutive days during the last third of the pregnancy. The ability of isolated perfused fetal rabbit lungs to metabolize arachidonic acid (AA) was studied on the 31st day of the pregnancy. After the infusion of 14C-AA (100 nmol) into the pulmonary circulation about 10% of the radioactivity was found in the nonrecirculating perfusion effluent and about 80% was incorporated into the lung lipids. Aspirin pretreatment of the rabbits inhibited the formation of AA metabolites in the lungs of their fetuses. The inhibition was clear when the metabolites of AA were extracted from the perfusion effluent at pH 7.4 (mainly lipoxygenase products) but a slight inhibition was also seen in the amounts of some metabolites extracted at pH 4.5 (cyclo-oxygenase products). When aspirin (1 mM) was infused simultaneously with AA into the pulmonary circulation the inhibition of AA metabolism was nearly complete. Aspirin pretreatment of the pregnant rabbits caused a slight increase in the amount of 14C-AA incorporated into some of the phospholipid and neutral lipid fractions of the perfused fetal lungs. Aspirin pretreatment clearly inhibited the TXB2 formation during clotting in the blood of maternal rabbits but not significantly in the blood of their fetuses.
D000818:Animals; D001095:Arachidonic Acids / Q000378:metabolism*; D001241:Aspirin / Q000494:pharmacology*; D002855:Chromatography, Thin Layer; D016861:Cyclooxygenase Inhibitors; D005260:Female; D005333:Fetus / Q000378:metabolism*; D050356:Lipid Metabolism; D008168:Lung / Q000187:drug effects* / Q000378:metabolism; D008431:Maternal-Fetal Exchange; D011247:Pregnancy; D011817:Rabbits; D013929:Thromboxane B2 / Q000097:blood
D001095:Arachidonic Acids; D016861:Cyclooxygenase Inhibitors; D013929:Thromboxane B2; D001241:Aspirin