ENHANCED ANALGESIA AND SUPPRESSION OF PLASMA BETA-ENDORPHIN BY THE S(-ISOMER OF IBUPROFEN())

Citation
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
Citations number
19
Categorie Soggetti
Pharmacology & Pharmacy
ISSN journal
00099236
Volume
63
Issue
6
Year of publication
1998
Pages
694 - 701
Database
ISI
SICI code
0009-9236(1998)63:6<694:EAASOP>2.0.ZU;2-2
Abstract
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.