Bruehl Stephen, Chung Ok Yung, Ward Pamela, Johnson Benjamin, McCubbin James A
Department of Anesthesiology, Vanderbilt University School of Medicine, Nashville, TN 37212, USA.
Pain. 2002 Nov;100(1-2):191-201. doi: 10.1016/s0304-3959(02)00295-6.
Resting blood pressure is inversely correlated with acute pain sensitivity in healthy normotensives. This study tested: (1) whether endogenous opioid activity is necessary for this adaptive relationship to occur, (2) whether this relationship is altered in chronic low back pain (LBP), and (3) whether endogenous opioid dysfunction underlies any such alterations. Fifty-one pain-free normotensives and 44 normotensive chronic LBP sufferers received opioid blockade (8 mg naloxone i.v.) or placebo blockade (saline) in randomized, counterbalanced order in separate sessions. During each session, subjects participated in a 1-min finger pressure (FP) pain task followed by an ischemic (ISC) forearm pain task. Among pain-free normotensives, elevated resting systolic (SBP) and diastolic (DBP) blood pressure were associated with significantly higher ISC pain thresholds (P values <0.05). Elevated SBP was also associated with significantly lower FP pain ratings (P<0.05). Opioid blockade had no significant effect on the BP-pain relationships detected (P values >0.10). In combined groups analyses, a significant subject typexSBP interaction (P<0.005) was found on ISC pain threshold: elevated SBP was associated with higher pain threshold in pain-free controls, but with lower pain threshold in LBP subjects. Although subject typexBP interactions on FP and ISC pain ratings were not significant, inclusion of LBP subjects in these analyses resulted in the overall relationship between BP and pain sensitivity becoming positive (P values <0.05). Opioid blockade exerted no significant main or interaction effects in these combined groups analyses (p values >0.10). Higher DBP was associated with greater clinical pain intensity among the LBP subjects (P<0.001). Overall, these results suggest: (1) endogenous opioids do not mediate the inverse relationship between resting blood pressure and acute pain sensitivity in pain-free normotensives; (2) the BP-pain sensitivity relationship is altered in chronic pain, suggesting dysfunction in pain regulatory systems, and (3) these alterations are not related to opioid dysfunction.
在健康的血压正常者中，静息血压与急性疼痛敏感性呈负相关。本研究检验了：（1）内源性阿片类物质活性对于这种适应性关系的发生是否必要；（2）这种关系在慢性下腰痛（LBP）患者中是否改变；（3）内源性阿片类物质功能障碍是否是任何此类改变的基础。51名无疼痛的血压正常者和44名血压正常的慢性LBP患者在不同的时段以随机、平衡的顺序接受阿片类物质阻断（静脉注射8mg纳洛酮）或安慰剂阻断（生理盐水）。在每个时段，受试者先参与1分钟的手指压力（FP）疼痛任务，随后进行缺血性（ISC）前臂疼痛任务。在无疼痛的血压正常者中，静息收缩压（SBP）和舒张压（DBP）升高与ISC疼痛阈值显著升高相关（P值<0.05）。SBP升高还与FP疼痛评分显著降低相关（P<0.05）。阿片类物质阻断对检测到的血压与疼痛的关系无显著影响（P值>0.10）。在合并组分析中，发现ISC疼痛阈值存在显著的受试者类型×SBP交互作用（P<0.005）：SBP升高在无疼痛的对照组中与较高的疼痛阈值相关，但在LBP受试者中与较低的疼痛阈值相关。尽管受试者类型×血压对FP和ISC疼痛评分的交互作用不显著，但在这些分析中纳入LBP受试者导致血压与疼痛敏感性之间的总体关系变为正相关（P值<0.05）。在这些合并组分析中，阿片类物质阻断未产生显著的主效应或交互效应（P值>0.10）。在LBP受试者中，较高的DBP与更大的临床疼痛强度相关（P<0.001）。总体而言，这些结果表明：（1）内源性阿片类物质不介导无疼痛的血压正常者中静息血压与急性疼痛敏感性之间的负相关关系；（2）血压与疼痛敏感性的关系在慢性疼痛中发生改变，提示疼痛调节系统功能障碍；（3）这些改变与阿片类物质功能障碍无关。
