Characteristics of the aggregation of platelets and the formation of prostaglandins (PGs) in rat

Abstract

Unlike human platelets, arachidonic acid (AA) at 1 m m could not induce aggregation of citrated rat platelets. However, preincubation of platelet rich plasma (PRP) with AA (1 m m) enhanced the aggregation induced by collagen suspension or adenosine diphosphate (ADP), and this enhancement was abolished by the preincubation of PRP with indomethacin. Arachidonic acid at a higher concentration (6 m m) induced aggregation, but it was not attenuated by the preincubation of indomethacin or imidazole indicating that this aggregation may not be augmented by PGs or their intermediates. Preincubation of PRP with imidazole neither abolished the enhancement of ADP-induced or collagen-induced aggregation by AA (1 m m), nor attenuated the aggregation induced by ADP or collagen alone; but it inhibited the synthesis of thromboxane (TX) by more than 90%. This suggested that rat platelets are not as sensitive to aggregation by TXA 2 as human platelets. Preincubation of mepacrine hydrochloride (0.5 m m) with PRP prevented the induction of aggregation by ADP or collagen, but it did not inhibit the aggregation by AA (6 m m). Mepacrine also inhibited the formation of PGs and TXA 2. Unlike citrated platelets, arachidonic acid even at 0.25 m m induced aggregation of heparinized rat platelets, implying that the aggregation of rat platelet is more dependent on calcium concentration than human platelets.