The effect of cutaneous mast cell degranulation on sensitivity to heat
The effect of cutaneous mast cell degranulation on sensitivity to heat
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DOI：
10.1007/s00011-004-1263-3
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发表时间：
2004-06-01
影响因子：
6.7
通讯作者：
Drummond, PD
中科院分区：
文献类型：
--
作者：
Drummond, PD
目的：确定皮肤肥大细胞炎症介质的消耗是否影响皮肤对热的敏感性或由辣椒素或去甲肾上腺素引起的热痛觉过敏。受试者：10名健康男性。方法和结果：通过离子电渗疗法将化合物48/80引入前臂。化合物 48/80 离子电渗疗法部位的风团经过四次预处理后消退，与肥大细胞脱粒一致。化合物 48/80 部位周围皮肤中的耀斑在第一次预处理后减少，但在风团消失后在一定程度上持续存在，表明肥大细胞激活过程中产生的试剂（例如，脱粒肥大细胞释放的细胞因子或脂氧合酶产物）触发了残留耀斑。第二次施用化合物48/80后，对热的敏感性增加，这可能是由于浸润白细胞释放的炎症介质对热伤害感受器的敏化所致。然而，化合物48/80预处理抑制了辣椒素的痛觉过敏作用。用化合物48/80预处理并不能阻止去甲肾上腺素的轴突反射性血管舒张或去甲肾上腺素在辣椒素处理的皮肤中的痛觉过敏作用。结论：两种机制可以解释化合物48/80预处理对辣椒素痛觉过敏作用的抑制作用。首先，肥大细胞产物可以部分介导辣椒素的痛觉过敏作用。其次，肥大细胞激活过程中产生的试剂（例如脂氧合酶产物）使香草酸受体亚型 1 部分脱敏，可以掩盖辣椒素的痛觉过敏作用。肥大细胞似乎不介导去甲肾上腺素的痛觉过敏作用。
Objective:To determine whether depletion of inflammatory mediators from cutaneous mast cells influences cutaneous sensitivity to heat or the thermal hyperalgesia provoked by capsaicin or noradrenaline.Subjects:Ten healthy men.Methods and results:Compound 48/80 was introduced by iontophoresis into the forearm. Wheals at the site of compound 48/80 iontophoresis subsided over four pre-treatments, consistent with mast cell degranulation. Flares in the skin surrounding the compound 48/80 sites decreased after the first pre-treatment but persisted to some extent after wheals had disappeared, suggesting that a reagent produced during mast cell activation (e.g., a cytokine or lipoxygenase product released from degranulated mast cells) triggered a residual flare. Sensitivity to heat increased after the second administration of compound 48/80, possibly due to sensitization of thermal nociceptors by inflammatory mediators released from infiltrating leukocytes. However, the compound 48/80 pre-treatment inhibited the hyperalgesic effect of capsaicin. Pre-treatment with compound 48/80 did not prevent axon-reflex vasodilatation to noradrenaline or the hyperalgesic effect of noradrenaline in capsaicin-treated skin.Conclusions:Two mechanisms could account for the inhibitory effect of the compound 48/80 pre-treatment on the hyperalgesic effect of capsaicin. First, mast cell products could partly mediate the hyperalgesic effect of capsaicin. Second, partial desensitization of the vanilloid receptor subtype-1 by a reagent produced during mast cell activation (e.g., a lipoxygenase product) could mask the hyperalgesic effect of capsaicin. Mast cells do not appear to mediate the hyperalgesic effect of noradrenaline.