Why the study?
Does tiaramide inhibit platelet aggregation and alter electrophoretic mobility in rabbit platelets compared to aspirin and indomethacin?
Does tiaramide inhibit platelet aggregation and alter electrophoretic mobility in rabbit platelets compared to aspirin and indomethacin?
Tiaramide inhibits ADP- and collagen-induced platelet aggregation in rabbits through a mechanism independent of prostaglandin synthesis.
Tiaramide's prostaglandin-independent antiplatelet activity in rabbits is hypothesis-generating; leaves open translation to human thrombosis prevention.
Effects of tiaramide, aspirin and indomethacin were studied on rabbit platelet aggregation in vivo and on platelet electrophoretic mobility. When tiaramide (6 mg/kg), aspirin (30 mg/kg) or indomethacin (1.3 mg/kg) was injected into the ear vein of rabbit during 60 sec, tiaramide only inhibited ADP-induced aggregation, 20 min after the injection. All three drugs prevented collagen-induced aggregation 20 and 120 min after the injection. Tiaramide and aspirin prevented aggregation 24 hours later. The inhibitory effects on the aggregation of tiaramide are presumably independent of prostaglandin synthesis, because malondialdehyde (a metabolite of PGG2) production was not influenced. Tiaramide reduced cyclic AMP levels in platelets after 20 min incubation, despite the ability of this agent to inhibit platelet aggregation. Tiaramide, aspirin and indomethacin per se has no effect on platelet electrophoretic mobility, while tiaramide prevented the decrease in the mobility produced by ADP. Tiaramide and aspirin also depressed the decrease in the mobility produced by collagen.
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Takano et al. (1980) studied this question.
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