Time course of UVA- and UVB-induced inflammation and hyperalgesia in human skin
Time course of UVA- and UVB-induced inflammation and hyperalgesia in human skin
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DOI：
10.1053/eujp.1998.0106
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发表时间：
1999-01-01
期刊：
影响因子：
--
通讯作者：
Schmelz, M
中科院分区：
文献类型：
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作者：
Hoffmann, RT;Schmelz, M
在10名健康受试者中研究了UVA（16.8和36 J/cm（2））和UVB（最小红斑阈值的1倍和3倍）照射后痛觉过敏和红斑的剂量依赖性和时间过程。用UVA或UVB光照射大腿腹侧的皮肤贴片（直径1.5 cm）。在照射后1、6、12、24、48和96 h检测充血（激光多普勒血流仪，红外热成像）、辐射热刺激的热痛觉过敏和控制冲击刺激的机械痛觉过敏。剂量依赖性迟发性充血和痛觉过敏只由UVB照射引起。UVB诱导的血流量增加在照射后12 h达到峰值，96 h恢复正常。虽然表面血流量，激光多普勒血流仪测量，增加了8倍，没有显着增加皮肤温度检测使用红外热成像。机械和热痛觉过敏的发展被延迟，并在24和48小时之间达到平台。与UVB相反，高达36 J/cm（2）的UVA照射足以产生强烈的皮肤晒黑，不会引起明显的痛觉过敏或延迟性充血。得出的结论是，UVB照射而不是UVA照射是亚急性热痛敏和机械痛敏的合适实验模型。红斑和痛觉过敏的不同时间过程表明，负责血管舒张的炎症介质与那些诱导痛觉过敏是不相同的。
Dose-dependency and time course of hyperalgesia and erythema following UVA (16.8 and 36 J/cm(2)) and UVB (one and three times the minimum erythema threshold) irradiation was investigated in 10 healthy human subjects. Skin patches (1.5 cm in diameter) on the ventral side of the upper leg were irradiated with UVA or UVB light. Hyperaemia (Laser Doppler flowmetry, infrared thermography), thermal hyperalgesia to radiant heat stimuli, and mechanical hyperalgesia to controlled impact stimuli were tested at 1, 6, 12, 24, 48 and 96 h after irradiation. Dose-dependent delayed hyperaemia and hyperalgesia was induced only by UVB irradiation. UVB-induced increase in blood flow peaked at 12 h after irradiation and normalized by 96 h. Although superficial blood flow, as measured by Laser Doppler flowmetry, increased up to eight-fold, no significant increase of skin temperature was detected using infrared thermography. Development of mechanical and thermal hyperalgesia was delayed and reached a plateau between 24 and 48 h. In contrast to UVB, UVA irradiation of up to 36 J/cm(2), sufficient to produce intense tanning of the skin, did not induce significant hyperalgesia or delayed hyperaemia. It is concluded that UVB- but not UVA-irradiation is a suitable experimental model of subacute thermal and mechanical hyperalgesia. The different time courses of erythema and hyperalgesia indicate that inflammatory mediators responsible for vasodilatation are not identical with those inducing hyperalgesia.