Opioid treatment of experimental pain activates nuclear factor-kappaB.

Opioid treatment of experimental pain activates nuclear factor-kappaB. - 2015

CONCLUSIONS: The combination of acute pain with opioids, as occurs in clinical situations, activates a key transcription factor involved in proinflammatory responses. DESIGN: NF-kappaB activation was compared within-subjects following four randomly ordered experimental sessions of opioid-only (intravenous fentanyl 1 mug/kg), painonly (cold-pressor), opioid + pain, and a resting condition. INTERVENTIONS: Following exposure to treatment (fentanyl administration and/or cold-pressor pain), blood samples for NF-kappaB analysis were obtained. MAIN OUTCOME MEASURES: Intracellular levels of activated NF-kappaB, in unstimulated and stimulated peripheral blood mononuclear cells at 15 and 30 minutes. OBJECTIVE: To determine the independent and combined effects of pain and opioids on the activation of an early marker of inflammation, nuclear factor-kappaB (NF-kappaB). PARTICIPANTS: Twenty-one (11 female) healthy controls. RESULTS: Neither pain nor opioid administration alone effected NF-kappaB levels in cell populations; however, the combination of treatments induced significant increases of NF-kappaB in stimulated peripheral blood mononuclear cell, lymphocytes, and monocytes. SETTING: University General Clinical Research Center.


English

1551-7489


*Analgesics, Opioid/tu [Therapeutic Use]
*Fentanyl/tu [Therapeutic Use]
*NF-kappa B/bl [Blood]
*Pain/dt [Drug Therapy]
Adult
Female
Follow-Up Studies
Healthy Volunteers
Humans
Injections, Intravenous
Male
Monocytes/de [Drug Effects]
Pain/bl [Blood]
Signal Transduction/de [Drug Effects]


MedStar Health Research Institute


Journal Article
Observational Study
Randomized Controlled Trial
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Powered by Koha