Ra. Dionne et L. Mccullagh, ENHANCED ANALGESIA AND SUPPRESSION OF PLASMA BETA-ENDORPHIN BY THE S(-ISOMER OF IBUPROFEN()), Clinical pharmacology and therapeutics, 63(6), 1998, pp. 694-701
Background: Peripheral nociceptive barrage after tissue injury results
in acute pain and a variety of physiologic responses, including pitui
tary secretion of beta-endorphin, This study evaluated whether adminis
tration of the pharmacologically active S(+)-isomer of ibuprofen suppr
esses acute pain and plasma beta-endorphin levels in the oral surgery
model of acute pain, Methods: Subjects in a single-dose, double-blind,
parallel-group study received either 200 mg S(+)-ibuprofen, 400 mg S(
+)-ibuprofen, 400 mg racemic ibuprofen, or placebo. Both doses of S(+)
-ibuprofen resulted in significantly greater analgesia over the first
60 minutes in comparison to racemic ibuprofen and placebo; the 400 mg
dose of S(+)-ibuprofen also produced greater analgesia at 2 and 3 hour
s. Plasma levels of immunoreactive beta-endorphin decreased over time
coincident with the onset of analgesia in all groups but were signific
antly less than placebo after both doses of S(+)-ibuprofen from 30 to
120 minutes, Conclusions: These findings show that, compared with race
mic ibuprofen, administration of the S(+)-isomer of ibuprofen results
in faster analgesic onset, greater peak analgesia, similar duration of
action, and a low incidence of adverse effects, while suppressing noc
iceptive activation of the pituitary-adrenal axis.