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The relationship between resting blood pressure and acute pain sensitivity: effects of chronic pain and alpha-2 adrenergic blockade

机译:静息血压与急性疼痛敏感性之间的关系:慢性疼痛和α-2肾上腺素能阻滞的影响

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This study tested for alpha-2 adrenergic mediation of the inverse relationship between resting blood pressure and acute pain sensitivity in healthy individuals. It also replicated limited prior work suggesting this inverse blood pressure/pain association is altered in chronic pain, and provided the first test of whether chronic pain-related changes in alpha-2 adrenergic function contribute to these alterations. Resting blood pressure was assessed in 32 healthy controls and 24 chronic low back pain participants prior to receiving placebo or an intravenous alpha-2 adrenergic receptor antagonist (yohimbine hydrochloride, 0.4 mg/kg) in a randomized crossover design. Participants experienced three acute pain tasks during both sessions. A significant Systolic Blood Pressure × Participant Type × Drug interaction on finger pressure McGill Pain Questionnaire-Sensory ratings (P < .05) reflected significant hyperalgesic effects of yohimbine in chronic pain participants with lower systolic blood pressures (P < .05) but not those with higher systolic pressures, and no significant effects of yohimbine in controls regardless of blood pressure level. A Drug × Systolic Blood Pressure interaction on finger pressure visual analog scale unpleasantness indicated the inverse blood pressure/pain association was significantly stronger under yohimbine relative to placebo (P < .05). Significant Participant Type × Systolic Blood Pressure interactions (P’s < .05) were noted for finger pressure visual analog scale pain intensity and unpleasantness, ischemic pain threshold, and heat pain threshold, reflecting absence or reversal of inverse blood pressure/pain associations in chronic pain participants. Results suggest that blood pressure-related hypoalgesia can occur even when alpha-2 adrenergic systems are blocked. The possibility of upregulated alpha-2 adrenergic inhibitory function in chronic pain patients with lower blood pressure warrants further evaluation.
机译:该研究测试了健康个体中静息血压与急性疼痛敏感性之间的反比关系的α-2肾上腺素能介导。它还重复了有限的先前工作,表明在慢性疼痛中这种反向的血压/疼痛关联得到了改变,并提供了关于α-2肾上腺素功能的慢性疼痛相关变化是否促成这些变化的第一个试验。在接受随机对照试验的安慰剂或静脉注射α-2肾上腺素能受体拮抗剂(盐酸育亨宾,0.4 mg / kg)之前,对32位健康对照和24位慢性下腰痛参与者的静息血压进行了评估。在这两个阶段中,参与者经历了三个急性疼痛任务。显着的收缩压×参与者类型×药物对手指压力的相互作用麦吉尔疼痛问卷调查的感官评分(P <.05)反映了育亨宾对收缩压较低(P <.05)的慢性疼痛参与者有明显的镇痛作用,但并非如此收缩压较高,并且无论血压水平如何,育亨宾对对照组均无明显影响。在手指压力视觉模拟量表上,药物×收缩压的交互作用令人不愉快,这表明育亨宾组的逆血压/疼痛关联明显强于安慰剂(P <.05)。对于手指压力视觉模拟量表疼痛强度和不适,缺血性疼痛阈值和热痛阈值,注意到了重要的参与者类型×收缩压相互作用(P <.05),反映了慢性疼痛中不存在或逆转反向的血压/疼痛关联参与者。结果表明,即使α-2肾上腺素系统被阻滞,也可能发生与血压有关的痛觉过敏。血压较低的慢性疼痛患者中α-2肾上腺素抑制功能上调的可能性值得进一步评估。

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