Abstract

Arachidonic Acid (AA) infusion in the ex vivo cat model was performed to determine the effects of the products produced from the metabolism of AA on the disaggregation of platelets accumulated on a rabbit Achilles tendon. Apparent peak blood levels of both prostacyclin (PGI2) and thromboxane (TXA2) were noted 4-8 minutes post initiation of AA infusion (1.0 mpk, i.v.). Plasma levels of PGI2 and TXA2 were determined by radioimmunoassay. Significant platelet disaggregation was noted 6-8 minutes post AA infusion with peak effects attained at 20-24 minutes. In other experiments no disaggregation occurred when AA was infused at 0.5 mg/kg. PGI2 infused in the same animal model at 14 μg/kg was detected in peak levels within 2 minutes after infusion and disappeared rapidly thereafter. Disaggregation of accumulated platelets following PGI2 infusion occurred immediately after the completion of infusion and continued over the 20 minute observation period. This data shows that AA infused into the cat can be converted to both PGI2 and TXA2 and that at 1.0 mg/kg AA, sufficient PGI2 is produced to result in platelet disaggregation even in the presence of elevated TXA2 levels.

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