Thomsen J S, Sonne M, Benfeldt E, Jensen S B, Serup J, Menné T
Department of Dermatology, Gentofte Hospital, University of Copenhagen, Niels Andersens Vej 65, DK-2900 Hellerup, Denmark.
Br J Dermatol. 2002 May;146(5):792-800. doi: 10.1046/j.1365-2133.2002.04722.x.
Investigations of pruritogenic substances in humans have involved intradermal injections in normal skin; itching of inflamed skin has been little studied.
To develop an itch model with provocation of itch in experimentally inflamed skin as well as in normal skin, using subjects as self-controls.
In 32 non-atopic volunteers aged 21-30 years, the skin of five selected test sites on one volar forearm was pretreated for 24 h with large Finn chambers containing 1% sodium lauryl sulphate (SLS) used as a standard contact irritant to induce inflammation. Twenty microlitres of different pruritogenic substances [histamine, substance P, neurokinin A, neurokinin B, trypsin, platelet-activating factor (PAF) and serotonin] and saline as control were injected intradermally into the inflamed test sites and in corresponding non-treated sites on the opposite forearm. The test individuals scored itch intensity on a visual analogue scale for 20 min, and weal area was then measured. :
Histamine and substance P induced itch in both normal and inflamed skin compared with a saline reference. Neurokinin A, trypsin, PAF and serotonin only elicited itch in normal skin, and neurokinin B neither elicited itch in normal skin nor in inflamed skin. Itch was induced in normal and SLS-inflamed skin to a similar magnitude. However, weal area after histamine was significantly (P < 0.001) larger in inflamed skin when compared with normal skin.
Histamine and substance P elicited itch to the same degree in normal skin and inflamed skin pretreated with SLS despite a stronger weal response in inflamed skin. Mediators present in inflamed skin did not potentiate itch, a c-fibre-mediated neuronal response. The weal reaction is based on enhanced vascular permeability (protein extravasation). A greater skin perfusion in inflamed skin may therefore have increased the weal size. We propose an experimental model in humans for testing of itch involving both normal and inflamed skin. The model has the potential for use in evaluating new topical and systemic treatments of itch.
对人类致痒物质的研究涉及在正常皮肤内进行皮内注射;对炎症皮肤瘙痒的研究较少。
以受试者自身作为对照,建立一个在实验性炎症皮肤以及正常皮肤中诱发瘙痒的瘙痒模型。
在32名年龄在21 - 30岁的非特应性志愿者中,用含有1%月桂醇硫酸酯钠(SLS)的大芬氏小室对一侧前臂掌面五个选定的测试部位的皮肤进行预处理24小时,SLS用作标准接触性刺激物以诱导炎症。将20微升不同的致痒物质[组胺、P物质、神经激肽A、神经激肽B、胰蛋白酶、血小板活化因子(PAF)和5-羟色胺]以及作为对照的生理盐水皮内注射到炎症测试部位和对侧前臂相应的未处理部位。测试个体在视觉模拟量表上对瘙痒强度进行20分钟评分,然后测量风团面积。
与生理盐水对照相比,组胺和P物质在正常皮肤和炎症皮肤中均诱发瘙痒。神经激肽A、胰蛋白酶、PAF和5-羟色胺仅在正常皮肤中引起瘙痒,而神经激肽B在正常皮肤和炎症皮肤中均未引起瘙痒。在正常皮肤和SLS诱导的炎症皮肤中诱发的瘙痒程度相似。然而,与正常皮肤相比,炎症皮肤中组胺注射后的风团面积显著更大(P < 0.001)。
组胺和P物质在正常皮肤和用SLS预处理的炎症皮肤中引起的瘙痒程度相同,尽管炎症皮肤中的风团反应更强。炎症皮肤中存在的介质并未增强瘙痒,瘙痒是一种由c纤维介导的神经元反应。风团反应基于血管通透性增强(蛋白质外渗)。因此,炎症皮肤中更大的皮肤灌注可能增加了风团大小。我们提出了一种在人类中用于测试涉及正常皮肤和炎症皮肤瘙痒的实验模型。该模型有潜力用于评估瘙痒的新局部和全身治疗方法。