Abstract
Summary
The bisenoic prostaglandin precursor, arachidonic acid (AA), in a single dose intravenously, produced a marked vasodepres-sor response in dogs, and a weak and variable effect on myocardial contractility. This response differed from the vasodepressor effect of PGE2 in that the onset of effect was delayed (15 sec for AA, 4.5 sec for PGE2) and PGE2 always caused a pronounced increase in myocardial contractility. Arachidonic acid caused thrombocytopenia and increased aggregability of platelets. All AA effects were inhibited by aspirin. The monoenoic prostaglandin precursor, dihomo-γ-linolenic acid, in doses equivalent to that of AA, had no effects. The data suggest that AA exerts its effects through conversion to an intermediate in the biosynthesis of PGE2 and not PGE2 itself.
This work was supported, in part, by the Educational Foundation of America.
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