CUTANEOUS HYPERALGESIA - CONTRIBUTIONS OF THE PERIPHERAL AND CENTRAL NERVOUS SYSTEMS TO THE INCREASE IN PAIN SENSITIVITY AFTER INJURY
CUTANEOUS HYPERALGESIA - CONTRIBUTIONS OF THE PERIPHERAL AND CENTRAL NERVOUS SYSTEMS TO THE INCREASE IN PAIN SENSITIVITY AFTER INJURY
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DOI：
10.1016/0006-8993(87)91359-x
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发表时间：
1987-02-24
期刊：
影响因子：
2.9
通讯作者：
MELZACK, R
中科院分区：
文献类型：
--
作者：
CODERRE, TJ;MELZACK, R
这项研究评估了外周和中枢神经系统在受伤后痛觉过敏（疼痛敏感性增加）发展中的作用。进行实验以检查 C 纤维传入神经、脊髓和交感传出神经对热损伤引起的大鼠炎症、原发性痛觉过敏和牵涉痛觉过敏的作用。表明了外周机制，因为通过用局部辣椒素阻断 C 纤维传入，原发性痛觉过敏和热损伤后的炎症均显着减弱。此外，还表明了一个中心机制，因为通过脊髓麻醉或胍乙啶阻断交感神经传出，可以防止痛觉过敏扩散到热损伤对侧的爪子。中枢机制的进一步作用被指出，因为称为痛觉过敏。sbd。先前遭受热损伤的去神经肢体的自残（自残）的增强。sbd。通过脊髓麻醉或鞘内辣椒素+胍乙啶联合阻断 C 纤维传入和交感传出而减少。结果强烈表明热损伤后的痛觉过敏取决于脊髓活动的增加。然而，先前未受过损伤的大鼠的自切术不受脊髓麻醉或鞘内辣椒素的影响。这表明脊髓过度活跃虽然在热损伤后的痛觉过敏中发挥作用，但并不是神经损伤后产生疼痛和痛觉过敏的关键因素。
This study assesses the contributions of the peripheral and central nervous systems in the development of hyperalgesia (increased pain sensitivity) after an injury. Experiments were carried out to examine the role of C-fiber afferents, the spinal cord and sympathetic efferents on inflammation, primary hyperalgesia and referred hyperalgesia produced in rats by a heat injury. A peripheral mechanism was indicated since both primary hyperalgesia and inflammation after a heat injury were significantly attenuated by blocking C-fiber afferents with local capsaicin. In addition, a central mechanism was indicated since the spread of hyperalgesia to the paw contralateral to a heat injury was prevented by either spinal anesthesia or the blocking of sympathetic efferents by guanethidine. A further role for central mechanisms was indicated since referred hyperalgesia.sbd.the enhancement of self-mutilation (autotomy) of a denervated limb which had previously sustained a heat injury.sbd.was reduced by spinal anesthesia or a combined blocking of C-fiber afferents and sympathetic efferents with intrathecal capsaicin + guanethidine. The results strongly suggest that referred hyperalgesia after a heat injury is dependent on increased spinal cord activity. However, autotomy in rats that did not undergo a previous injury was unaffected by either spinal anesthesia or intrathecal capsaicin. This suggests that spinal cord hyperactivity, although it plays a role in hyperalgesia following a heat injury, is not a crucial factor in producing pain and hyperalgesia after a nerve injury.