Repeated sound stress enhances inflammatory pain in the rat
Repeated sound stress enhances inflammatory pain in the rat
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DOI：
10.1016/j.pain.2005.03.040
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发表时间：
2005-07-01
期刊：
影响因子：
7.4
通讯作者：
Levine, JD
中科院分区：
文献类型：
--
作者：
Khasar, SG;Green, PG;Levine, JD
众所周知，急性应激可以产生抗痛觉，这种现象被称为应激性镇痛，但反复暴露在压力下可能会产生相反的效果。由于慢性疼痛综合征，如纤维肌痛和类风湿性关节炎，可能由慢性应激触发和/或加重，我们已经评估了反复应激对机械痛觉阈和炎症性痛觉过敏的影响。利用Randall-Selitto爪压试验量化大鼠的痛觉阈值，我们发现重复的非适应声应激增强了由强效炎症介质缓激肽引起的机械性痛觉过敏，在正常大鼠中，缓激肽通过刺激交感神经末梢释放前列腺素E-2间接产生痛觉过敏。直接作用的炎症介质前列腺素E-2诱导的痛觉过敏以及基线伤害阈值不受影响。肾上腺髓质切除或去神经，逆转声应激的影响。在声音应激动物中，缓激肽-痛觉过敏的发病潜伏期更快，不再受交感神经切除术的抑制，这与缓激肽对初级传入伤害感受器的直接作用是一致的。此外，肾上腺素的植入恢复了交感神经切除的非应激大鼠的缓激肽痛觉过敏，进一步支持了血浆中肾上腺素水平升高可以使初级传入神经对缓激肽敏感的观点。这些结果表明，应激诱导的炎症性痛觉过敏的增强与缓激肽诱导痛觉过敏的机制变化有关，从交感神经介导到交感神经独立。这种不依赖交感神经的机械性痛觉增强是由应激诱导的肾上腺素从肾上腺髓质释放介导的。(C) 2005国际疼痛研究协会。Elsevier B.V.版权所有。
While it is well established that acute stress can produce antinociception, a phenomenon referred to as stress-induced analgesia, repeated exposure to stress can have the opposite effect. Since, chronic pain syndromes, such as fibromyalgia and rheumatoid arthritis, may be triggered and/or exacerbated by chronic stress, we have evaluated the effect of repeated stress on mechanical nociceptive threshold and inflammatory hyperalgesia. Using the Randall-Selitto paw pressure test to quantify nociceptive threshold in the rat, we found that repeated non-habituating sound stress enhanced the mechanical hyperalgesia induced by the potent inflammatory mediator, bradykinin, which, in normal rats, produces hyperalgesia indirectly by stimulating the release of prostaglandin E-2 from sympathetic nerve terminals. Hyperalgesia induced by the direct-acting inflammatory mediator, prostaglandin E-2 as well as the baseline nociceptive threshold, were not affected. Adrenal medullectomy or denervation, reversed the effect of sound stress. In sound stressed animals, bradykinin-hyperalgesia had a more rapid latency to onset and was no longer inhibited by sympathectomy, compatible with a direct effect of bradykinin on primary afferent nociceptors. In addition, implants of epinephrine restored bradykinin-hyperalgesia in sympathectomized non-stressed rats, lending further support to the suggestion that increased plasma levels of epinephrine can sensitize primary afferents to bradykinin. These results suggest that stress-induced enhancement of inflammatory hyperalgesia is associated with a change in mechanism by which bradykinin induces hyperalgesia, from being sympathetically mediated to being sympathetically independent. This sympathetic-independent enhancement of mechanical hyperalgesia is mediated by the stress-induced release of epinephrine from the adrenal medulla. (C) 2005 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.