Journal of opioid management · 2015
Opioid treatment of experimental pain activates nuclear factor-κB.
СтатьяРандомизированное исследованиеПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Compton Peggy, Griffis Charles, Breen Elizabeth Crabb, Torrington Matthew, Sadakane Ryan, Tefera Eshetu, Irwin Michael R
Аннотация
OBJECTIVE: To determine the independent and combined effects of pain and opioids on the activation of an early marker of inflammation, nuclear factor-κB (NF-κB).
DESIGN: NF-κB activation was compared within-subjects following four randomly ordered experimental sessions of opioid-only (intravenous fentanyl 1 μg/kg), painonly (cold-pressor), opioid + pain, and a resting condition.
SETTING: University General Clinical Research Center.
PARTICIPANTS: Twenty-one (11 female) healthy controls.
INTERVENTIONS: Following exposure to treatment (fentanyl administration and/or cold-pressor pain), blood samples for NF-κB analysis were obtained.
MAIN OUTCOME MEASURES: Intracellular levels of activated NF-κB, in unstimulated and stimulated peripheral blood mononuclear cells at 15 and 30 minutes.
RESULTS: Neither pain nor opioid administration alone effected NF-κB levels in cell populations; however, the combination of treatments induced significant increases of NF-κB in stimulated peripheral blood mononuclear cell, lymphocytes, and monocytes.
CONCLUSIONS: The combination of acute pain with opioids, as occurs in clinical situations, activates a key transcription factor involved in proinflammatory responses.
DESIGN: NF-κB activation was compared within-subjects following four randomly ordered experimental sessions of opioid-only (intravenous fentanyl 1 μg/kg), painonly (cold-pressor), opioid + pain, and a resting condition.
SETTING: University General Clinical Research Center.
PARTICIPANTS: Twenty-one (11 female) healthy controls.
INTERVENTIONS: Following exposure to treatment (fentanyl administration and/or cold-pressor pain), blood samples for NF-κB analysis were obtained.
MAIN OUTCOME MEASURES: Intracellular levels of activated NF-κB, in unstimulated and stimulated peripheral blood mononuclear cells at 15 and 30 minutes.
RESULTS: Neither pain nor opioid administration alone effected NF-κB levels in cell populations; however, the combination of treatments induced significant increases of NF-κB in stimulated peripheral blood mononuclear cell, lymphocytes, and monocytes.
CONCLUSIONS: The combination of acute pain with opioids, as occurs in clinical situations, activates a key transcription factor involved in proinflammatory responses.