Abstract

Dihomo-γ-linolenate effectively prevented the irreversible aggregation of human platelets induced by collagen or epinephrine. Also, platelets from rats which received daily oral doses of dihomo-γ-linolenate showed significant reductions in platelet aggregatory responses to collagen and ADP which were attributable to increases in plasma and platelet ratios of dihomo-γ-linolenate to arachidonate. Similar results were obtained in rabbits. This data, together with that of enzymatic studies supports a hypothesis that oral ingestion of dihomo-γ-linolenate may effectively prevent arterial thrombosis in man by causing a redirection of platelet prostaglandin biosynthesis. Thus PGE 1 and its non-aggregatory endoperoxide intermediate (PGR 1) are formed at the expense of PGE 2 and LASS endoperoxide which together may induce platelet thrombus formation.

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