Acute painful stress and inflammatory mediator production.

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.