Effects of non-steroidal anti-inflammatory drugs on the in vivo synthesis of thromboxane and prostacyclin in humans.
Most NSAIDs seem to have inhibitory effects on the in vivo synthesis of both TxA2 and PGI2. However there are large differences in the duration of the inhibitory effects as shown in the table below. Aspirin, indomethacin, naproxen and piroxicam inhibit the second wave of platelet aggregation. This effect on platelet aggregation persists as long as each drug causes inhibition of TxA2 synthesis. Thus, inhibition of TxA2 synthesis is likely to be the reason for the effect of NSAIDs on platelet function. The lack of effect of paracetamol on TxA2 synthesis together with the lack of effect on platelet aggregation by paracetamol are in further support of this. [table: see text]
Drvota
V
V
Department of Clinical Chemistry and Blood Coagulation, Karolinska Hospital, Stockholm, Sweden.
Vesterqvist
O
O
Gréen
K
K
D000082:Acetaminophen / Q000494:pharmacology; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D001241:Aspirin / Q000494:pharmacology; D016861:Cyclooxygenase Inhibitors; D003864:Depression, Chemical; D011464:Epoprostenol / Q000096:biosynthesis*; D006801:Humans; D010894:Piroxicam / Q000494:pharmacology; D013928:Thromboxane A2 / Q000096:biosynthesis*; D013997:Time Factors
D000894:Anti-Inflammatory Agents, Non-Steroidal; D016861:Cyclooxygenase Inhibitors; D010894:Piroxicam; D000082:Acetaminophen; D013928:Thromboxane A2; D011464:Epoprostenol; D001241:Aspirin