PAIN REGULATORY SYSTEM DYSFUNCTION IN CHRONIC PAIN

静息血压(BP)升高与急性疼痛敏感性降低一致相关。IBIS心血管相关的抗伤害性感觉(部分由内源性阿片类药物介导)是健康个体对疼痛适应的重要组成部分。目前尚不清楚这些抗伤害机制是否在慢性疼痛患者中正常运行。先前的研究表明，慢性疼痛患者的内源性阿片水平存在缺陷，尽管对这些缺陷的功能影响(例如，止痛作用减弱)知之甚少。鉴于内源性阿片类药物在心血管相关的抗伤害感受中的中介作用以及在慢性疼痛条件下可能存在的阿片类药物缺陷，假设慢性疼痛患者的这些正常适应的心血管-疼痛调节关系将发生变化。这些研究的长期目标是探索慢性疼痛患者内源性疼痛调节系统功能障碍的本质。对慢性疼痛的机制的更好的理解有可能导致改善对慢性疼痛患者的治疗。这些研究的具体目的有三个：1)检查神经性和伤害性慢性疼痛患者与正常对照的静息血压和急性疼痛敏感性之间的关系，2)检查疼痛患者和正常对照组在静息血压和急性疼痛敏感性之间内源性阿片类药物调节程度的可能差异，以及3)检查慢性疼痛的内源性阿片类药物功能障碍是否为进行性的，因此与疼痛持续时间有关。60名慢性疼痛患者(研究L=神经性背痛，研究2=伤害性背痛)和60名健康对照组将接受一次实验室缺血性疼痛刺激，一次在安慰剂下，一次在阿片类药物阻断下加纳洛酮(随机平衡顺序)。在这两次会议中，静息血压将在基线上确定。疼痛患者也会在给药前后对他们的临床疼痛进行评分。预计控制组将显示静息血压和急性疼痛敏感性之间的显著负相关，这种相关性至少可被纳洛酮部分消除。预计疼痛患者的静息血压与急性疼痛反应之间没有相关性或正相关，并且对阿片类药物阻断没有反应。预计疼痛持续时间越长，阿片类药物阻断后BP/疼痛关系的变化越小。

Elevated resting blood pressure (BP) is consistently related to diminished acute pain sensitivity. Ibis cardIovascular-related antinociception (mediated in part by endogenous opioids) is an important component of adaptation to pain in healthy individuals. it is unknown whether these antinociceptive mechanisms operate normally in chronic pain patients. Previous research indicates deficits in endogenous opioid levels in chronic pain patients, although little is known about the functional impact (e.g., diminished analgesia) of these deficits. Given the mediating role of endogenous opioids in cardiovascular-related antinociception and likely opioid deficits in chronic pain conditions, it is hypothesized that chronic pain patients will display alterations in these normally adaptive cardiovascular-pain regulatory relationships. The long-term objective of these studies is to explore the nature of dysfunction in the endogenous pain regulatory systems of chronic pain patients. improved understanding of the mechanisms contributing to chronic pain has the potential to lead to improved treatment for chronic pain patients. The specific aims of these studies are threefold: 1) examine the relationship between resting blood pressure and acute pain sensitivity in both neuropathic and nociceptive chronic pain patients as contrasted to normals, 2) examine possible differences in degree of endogenous opioid mediation of the relationship between resting blood pressure and acute pain sensitivity across the pain patient and normal control subgroups, and 3) examine whether endogenous opioid dysfunction in chronic pain is progressive and therefore related to pain duration. Sixty chronic pain patients (study l=neuropathic back pain, study 2=nociceptive back pain) and 60 healthy controls will undergo a laboratory ischemic pain stimulus once under placebo and once under opioid blockade with naloxone (randomized, counterbalanced order). in both sessions, resting BP will be determined at baseline. Pain patients will also rate their clinical pain before and after drug administration. it is expected that controls will display significant negative correlations between resting BP and acute pain sensitivity, which is at least partially eliminated by naloxone. Pain patients are expected to demonstrate no correlation or a positive correlation between resting BP and acute pain responsiveness, and will be unresponsive to opioid blockade. Greater pain duration is expected to be associated with smaller changes in the BP/pain relationship in response to opioid blockade.