Platelet aggregation in rhesus macaques (Macaca mulatta) in response to short-term meloxicam administration

Abstract

NSAID administration is often chosen as a method of minimizing pain and discomfort for nonhuman primates. Of concern when using NSAID is the potential for decreased platelet aggregation due to the inhibition of cyclooxygenases 1 and 2. In both dogs and humans, the use of NSAID that are selective for cyclooxygenase 2, like meloxicam, minimizes the inhibition of platelet aggregation in comparison to nonselective NSAID, like aspirin, that inhibit both isoforms of cyclooxygenase. In this study, we measured platelet aggregation in rhesus macaques (n = 6) by using the impedance method on a multiple-electrode aggregometer at baseline, at 1 and 4 d after initiating treatment with aspirin or meloxicam, and after a washout period. There was no statistical difference between aggregation at baseline and after 1 or 4 d of meloxicam treatment, but platelet aggregation decreased after both 1 and 4 d of aspirin therapy. Our data suggest that clinically significant postoperative hemorrhage is unlikely in rhesus macaques briefly treated with meloxicam.

Figure 1.

ASPI-induced platelet aggregation (AUC; mean ± SEM) before drug administration (baseline), at 2 time points for aspirin and for meloxicam, and at 21 d after the final drug administration. *, Change from baseline was statistically significant (P < 0.05, 2-tailed t test) for aspirin after both 1 and 4 d of administration but not for meloxicam at either time point.