Key result
Ketorolac inhibited platelet aggregation and prostanoid biosynthesis to a significantly greater extent and for a longer period than azapropazone, which had an EC50 1000 times higher.
Why the study?
Does a single dose of azapropazone compared to ketorolac tromethamine have different effects on platelet function and prostanoid biosynthesis in healthy subjects?
Does a single dose of azapropazone compared to ketorolac tromethamine have different effects on platelet function and prostanoid biosynthesis in healthy subjects?
Azapropazone produces moderate, shorter-lasting inhibition of platelet function compared to ketorolac, which may be advantageous for post-operative analgesia.
Azapropazone may suit post-operative analgesia better due to milder platelet effects; hypothesis-generating for bleeding outcomes in patients.
The biosynthesis of thromboxane (TX) B2 and immunoreactive prostaglandin (PG) F2 alpha in clotting whole blood ex vivo as well as collagen-induced platelet aggregation were determined before and up to 72 h after intravenous injection of 600 mg azapropazone 2H2O and intramuscular injection of 30 mg ketorolac tromethamine in six healthy subjects. The drug doses were selected on the basis of comparable analgesic activity (maximal recommended analgesic dose). Both platelet aggregation and prostanoid biosynthesis were inhibited by racketorolac to a significantly greater extent and for a longer period of time than by azapropazone. Correlations between serum concentrations and the inhibitory effects on TXB2 biosynthesis were observed for both drugs. Using the sigmoidal Emax model the mean serum concentration of azapropazone inhibiting platelet TXB2 generation by 50% (EC50) was found to be 98.1 +/- 41.9 (s.d.) micrograms ml-1, a value 1000 times higher than that for rac-ketorolac. The moderate inhibition of platelet function by azapropazone as compared with rac-ketorolac might be an advantage with regard to its use as a post-operative analgesic.
No takes yet. Share an insight, caveat, or question.
Pallapies et al. (1994) studied Healthy subjects (n=6). Azapropazone vs. Ketorolac tromethamine (30 mg intramuscular injection) was evaluated on Biosynthesis of thromboxane (TX) B2, immunoreactive prostaglandin (PG) F2 alpha, and collagen-induced platelet aggregation. Ketorolac inhibited platelet aggregation and prostanoid biosynthesis to a significantly greater extent and for a longer period than azapropazone, which had an EC50 1000 times higher.