Abstract
Intact platelets from atherosclerotic rabbits release more thromboxane B 2 (TXB 2) and 12-hydroxyeicosatetraenoic acid (HETE) than platelets from normal rabbits following incubation with [ l4C]arachidonic acid (AA). In contrast, no difference is found between homogenates of platelets from normal and atherosclerotic animals. PGI 2 stimulates CAMP accumulation and inhibits TXB 2 formation more potently in intact platelets from atherosclerotic than from normal rabbits, but has no effect on AA metabolism in homogenised platelets.
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