School of Physiology and Pharmacology, University of Bristol, Medical Sciences Building, University Walk, Bristol BS8 1TD, UK Clinical Unit Cambridge, GlaxoSmithKline, Addenbrookes Hospital, Hills Road, Cambridge CB2 2GG, UK School of Veterinary Science, University of Bristol, Langford House, Langford, Bristol BS40 5DU, UK.
Pain. 2011 Dec;152(12):2844-2851. doi: 10.1016/j.pain.2011.09.015. Epub 2011 Oct 21.
Cutaneous inflammation induced by ultraviolet (UV) irradiation in the UV-B range has received significant recent interest as a translational inflammatory pain model. Changes in thermal and mechanical sensitivities in the area of primary hyperalgesia are well documented in both the rat and human UV-B models, but the occurrence of secondary mechanical hyperalgesia is controversial. We investigated the occurrence of secondary mechanical hyperalgesia in the rat UV-B model. Additionally, we investigated whether secondary hyperalgesia was enhanced by heat rekindling of UV-B-irradiated skin as a new rat inflammatory model of sensitisation with an enhanced central contribution. UV-B irradiation (1000 mJ/cm(2)) induced significant secondary mechanical hyperalgesia and allodynia that peaked at 48 h. Heat rekindling (45 °C stimulus for 5 min) of UV-B-irradiated skin at 24h further enhanced and prolonged this secondary mechanical hyperalgesia and allodynia, with a peak at 72 h. Heat rekindling also induced a significant mechanical hyperalgesia and allodynia on the contralateral hind paw, further suggesting the contribution of central sensitisation. Our data provide strong evidence for a central contribution in both the rat UV-B pain model and an enhanced contribution in the new model combining UV-B irradiation with heat rekindling. We also elucidate potential differences in the methods used by ourselves and others to obtain mechanical withdrawal thresholds in rats, which may explain the lack of secondary hyperalgesia in the rat UV-B model.
紫外线（UV）B 波段照射引起的皮肤炎症最近受到了广泛关注，成为一种转化性炎症疼痛模型。在大鼠和人类 UV-B 模型中，原发性痛觉过敏区域的热和机械敏感性变化都有详细记录，但继发性机械性痛觉过敏的发生存在争议。我们研究了大鼠 UV-B 模型中继发性机械性痛觉过敏的发生情况。此外，我们还研究了 UV-B 照射皮肤的热重燃是否会增强继发性痛觉过敏，作为一种具有增强中枢贡献的新型大鼠敏化炎症模型。UV-B 照射（1000 mJ/cm(2)）诱导显著的继发性机械性痛觉过敏和痛觉过敏，在 48 小时达到峰值。在 24 小时时，对 UV-B 照射皮肤进行热重燃（45°C 刺激 5 分钟）进一步增强和延长了这种继发性机械性痛觉过敏和痛觉过敏，在 72 小时达到峰值。热重燃还在对侧后爪引起明显的机械性痛觉过敏和痛觉过敏，进一步表明中枢敏化的贡献。我们的数据为大鼠 UV-B 疼痛模型中的中枢贡献以及将 UV-B 照射与热重燃相结合的新型模型中的增强贡献提供了有力证据。我们还阐明了我们自己和其他人在大鼠中获得机械退缩阈值的方法可能存在差异，这可能解释了大鼠 UV-B 模型中缺乏继发性痛觉过敏的原因。
