急性疼痛应激和炎症介质的产生。
Acute painful stress and inflammatory mediator production.
机构信息
UCLA Department of Anesthesiology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA.
出版信息
Neuroimmunomodulation. 2013;20(3):127-33. doi: 10.1159/000346199. Epub 2013 Feb 12.
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.
背景
在疼痛应激的情况下，促炎途径可能被激活，这被假设会使疼痛体验恶化，并使医学上脆弱的人群面临更高发病率的风险。
目的
评估疼痛和主观疼痛相关应激对促炎活性的影响。
方法
共有 19 名健康对照受试者接受了单次标准冷压疼痛测试（CPT）和无疼痛对照条件。测量疼痛和应激的指标，并将其与疼痛刺激后立即的炎症免疫反应[表达整合素分子 CD11a（CD811a）的 CD8+细胞、白细胞介素（IL）-1 受体激动剂（IL-1RA）和 IL-6]相关联，并与无疼痛条件下的反应进行比较。心率和平均动脉压作为交感神经刺激的指标进行测量。
结果
CPT 明显疼痛，并引起交感神经系统的激活。两种情况下 CD811a 均增加，但 CPT 后增加无统计学意义（p<0.06）。IL-1RA 在 CPT 后呈非统计学显著增加（p<0.07）。CPT 后 IL-6 的变化与对照条件下的反应明显不同（p<0.02）。
结论
这些发现表明 CP 急性疼痛可能影响促炎途径，可能通过与肾上腺素能激活相关的机制。
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