Opioid treatment of experimental pain activates nuclear factor-kappaB.

MedStar author(s):
Citation: Journal of Opioid Management. 11(2):115-25, 2015 Mar-Apr.PMID: 25901477Institution: MedStar Health Research InstituteForm of publication: Journal ArticleMedline article type(s): Journal Article | Observational Study | Randomized Controlled Trial | Research Support, N.I.H., Extramural | Research Support, Non-U.S. Gov'tSubject headings: *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]Year: 2015ISSN:
  • 1551-7489
Name of journal: Journal of opioid managementAbstract: 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.All authors: Breen EC, Compton P, Griffis C, Irwin MR, Sadakane R, Tefera E, Torrington MFiscal year: FY2015Digital Object Identifier: Date added to catalog: 2016-01-13
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Journal Article MedStar Authors Catalog Article 25901477 Available 25901477

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.

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