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Vol. 20, No. 3, 2013
Issue release date: April 2013
Section title: Original Paper
Neuroimmunomodulation 2013;20:127–133
(DOI:10.1159/000346199)

Acute Painful Stress and Inflammatory Mediator Production

Griffis C.A. · Crabb Breen E. · Compton P. · Goldberg A. · Witarama T. · Kotlerman J. · Irwin M.R.
aUCLA Department of Anesthesiology, bUCLA Cousins Center for Psychoneuroimmunology, cSemel Institute for Neuroscience and Department of Psychiatry and Biobehavioral Sciences, dDavid Geffen School of Medicine at UCLA, and eUCLA School of Nursing, Los Angeles, Calif., USA

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: 9/7/2012 8:44:28 AM
Accepted: 11/28/2012
Published online: 2/12/2013

Number of Print Pages: 7
Number of Figures: 1
Number of Tables: 3

ISSN: 1021-7401 (Print)
eISSN: 1423-0216 (Online)

For additional information: http://www.karger.com/NIM

Abstract

Background: Proinflammatory pathways may be activated under conditions of painful stress, which is hypothesized to worsen the experience of pain and place medically vulnerable populations at risk for increased morbidity. Objectives: To evaluate the effects of pain and subjective pain-related stress on proinflammatory activity. Methods: A total of 19 healthy control subjects underwent a single standard cold-pressor pain test (CPT) and a no-pain control condition. Indicators of pain and stress were measured and related to inflammatory immune responses [CD8+ cells expressing the integrin molecule CD11a (CD811a), interleukin (IL)-1 receptor agonist (IL-1RA), and IL-6] immediately following the painful stimulus and compared to responses under no-pain conditions. Heart rate and mean arterial pressure were measured as indicators of sympathetic stimulation. Results: CPT was clearly painful and generated an activation of the sympathetic nervous system. CD811a increased in both conditions, but with no statistically significantly greater increase following CPT (p < 0.06). IL-1RA demonstrated a non-statistically significant increase following CPT (p < 0.07). The change in IL-6 following CPT differed significantly from the response seen in the control condition (p < 0.02). Conclusions: These findings suggest that CP acute pain may affect proinflammatory pathways, possibly through mechanisms related to adrenergic activation.


  

Author Contacts

Assoc. Prof. Charles A. Griffis, CRNA, PhD
UCLA Department of Anesthesiology
200 Medical Plaza, Suite 660
Los Angeles, CA 90095 (USA)
E-Mail cgriffis55@gmail.com

  

Article Information

Received: September 7, 2012
Accepted after revision: November 28, 2012
Published online: February 12, 2013
Number of Print Pages : 7
Number of Figures : 1, Number of Tables : 3, Number of References : 58

  

Publication Details

Neuroimmunomodulation

Vol. 20, No. 3, Year 2013 (Cover Date: April 2013)

Journal Editor: Savino W. (Rio de Janeiro)
ISSN: 1021-7401 (Print), eISSN: 1423-0216 (Online)

For additional information: http://www.karger.com/NIM


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: 9/7/2012 8:44:28 AM
Accepted: 11/28/2012
Published online: 2/12/2013

Number of Print Pages: 7
Number of Figures: 1
Number of Tables: 3

ISSN: 1021-7401 (Print)
eISSN: 1423-0216 (Online)

For additional information: http://www.karger.com/NIM


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