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Abstract
14C-Arachidonic acid injected into the pulmonary circulation of isolated hamster lungs
was effectively incorporated into lung lipids. Once retained the radiolabel was relatively
stable but the release of radioactivity increased up to 10-fold when bovine serum
albumin (1 %) was added to the perfusate. This efflux of radioactivity was not blocked
by quinacrine, a phospholipase A2 inhibitor. In albumin experiments the released 14C-araehidonate griginated mainly from the phospholipid fraction in which phosphatidylcholine
was the main source of the released radioactivity.Pulmonary infusion of albumin had
no significant effect on the amount of 14C-arachidonic acid in the neutral lipid or free fatty acid fractions of perfused lungs.
In experiments with albumin about 80 % of the released radioactivity co-chromatographed
with unlabelled arachidonic acid whereas in the absence of albumin only about 20 %
of the released radioactivity was unmetabolized arachidonic acid. This study indicates
that albumin stimulates the release of arachidonic acid from isolated hamster lungs
and that the release is increased mainly from the phosphatidyl choline fraction.
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References
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© 1984 Published by Elsevier Inc.
