From the Prevention Science Institute and Department of Psychology (May), University of Oregon; Pain Consultants of Oregon (Kosek), Eugene, Oregon; Department of Neurobiology and Anatomy (Zeidan), Wake Forest School of Medicine, Winston-Salem, North Carolina; and Department of Psychology and Center for Translational Neuroscience (Berkman), University of Oregon, Eugene, Oregon.
Psychosom Med. 2018 Nov/Dec;80(9):807-813. doi: 10.1097/PSY.0000000000000580.
Studies have consistently shown that long-term meditation practice is associated with reduced pain, but the neural mechanisms by which long-term meditation practice reduces pain remain unclear. This study tested endogenous opioid involvement in meditation analgesia associated with long-term meditation practice.
Electrical pain was induced with randomized, double-blind, cross-over administration of the opioid antagonist naloxone (0.15-mg/kg bolus dose, then 0.2-mg/kg per hour infusion dose) with 32 healthy, experienced meditation practitioners and a standardized open monitoring meditation.
Under saline, pain ratings were significantly lower during meditation (pain intensity: 6.41 ± 1.32; pain unpleasantness: 3.98 ± 2.17) than at baseline (pain intensity: 6.86 ±1.04, t(31) = 2.476, p = .019, Cohen's d = 0.46; pain unpleasantness: 4.96 ±1.75, t(31) = 3.746, p = .001, Cohen's d = 0.68), confirming the presence of meditation analgesia. Comparing saline and naloxone revealed significantly lower pain intensity (t(31) = 3.12, p = .004, d = 0.56), and pain unpleasantness (t(31) = 3.47, p = .002, d = 0.62), during meditation under naloxone (pain intensity: 5.53 ± 1.54; pain unpleasantness: 2.95 ± 1.88) than under saline (pain intensity: 6.41 ± 1.32; pain unpleasantness: 3.98 ± 2.17). Naloxone not only failed to eliminate meditation analgesia but also made meditation analgesia stronger.
Long-term meditation practice does not rely on endogenous opioids to reduce pain. Naloxone's blockade of opioid receptors enhanced meditation analgesia; pain ratings during meditation were significantly lower under naloxone than under saline. Possible biological mechanisms by which naloxone-induced opioid receptor blockade enhances meditation analgesia are discussed.
研究一致表明，长期冥想练习与疼痛减轻有关，但长期冥想练习减轻疼痛的神经机制仍不清楚。本研究测试了内源性阿片参与与长期冥想练习相关的冥想镇痛。
通过随机、双盲、交叉给予阿片拮抗剂纳洛酮（0.15mg/kg 推注剂量，然后 0.2mg/kg/h 输注剂量），并结合标准化的开放监测冥想，对 32 名经验丰富的冥想练习者进行电刺激疼痛诱导。
在生理盐水条件下，冥想时的疼痛评分明显低于基线时（疼痛强度：6.41 ± 1.32；疼痛不适：3.98 ± 2.17）（t(31)=2.476，p=.019，Cohen's d=0.46；疼痛不适：4.96 ± 1.75，t(31)=3.746，p=.001，Cohen's d=0.68），证实了冥想镇痛的存在。比较生理盐水和纳洛酮发现，纳洛酮下冥想时的疼痛强度（t(31)=3.12，p=.004，d=0.56）和疼痛不适（t(31)=3.47，p=.002，d=0.62）明显低于生理盐水（疼痛强度：6.41 ± 1.32；疼痛不适：3.98 ± 2.17）。纳洛酮不仅没有消除冥想镇痛，反而使冥想镇痛更强。
长期冥想练习不依赖内源性阿片类物质来减轻疼痛。纳洛酮阻断阿片受体增强了冥想镇痛；纳洛酮下的疼痛评分明显低于生理盐水下。讨论了纳洛酮诱导的阿片受体阻断增强冥想镇痛的可能生物学机制。
