Tarayre J P, Aliaga M, Villanova G, Barbara M, Caillol V, Bru M, Lauressergues H
Arch Int Pharmacodyn Ther. 1984 May;269(1):153-66.
Picryl chloride applied to the ears of Swiss mice induced a clearcut primary irritation inflammation (maximal after 3 to 6 hr) and after contact sensitization performed 7 days before a delayed hypersensitivity reaction. Oxazolone produced only a weak primary irritation reaction. After contact sensitization in the same conditions as above, oxazolone induced an immune response that was already substantial 3 to 6 hr after the challenge and generally reached a maximum after 24 hr. We tried to alter these four types of inflammation (the primary irritation and delayed hypersensitivity to picryl chloride, and the 6-hr and 24-hr phases of hypersensitivity to oxazolone) by various types of compounds administered cutaneously or sytemically. Mepyramine, methysergide, cimetidine, disodium cromoglycate, phenylbutazone, and acetylsalicylic acid reduced to varying degrees after cutaneous application the primary irritation and the delayed hypersensitivity inflammation induced by picryl chloride. Methysergide was the only one of these drugs that on topical application clearly reduced the immune response to oxazolone (decrease in the 6-hr phase). After systemic administration, these same drugs had no effect on the four types of reaction. Both the corticosteroids tested (hydrocortisone acetate and desonide) reduced all the inflammations to various degrees and were always more active (particularly desonide) when applied topically than when administered systemically. On the other hand indomethacin, which inhibited all types of inflammation, was more active when administered systemically. Study of the kinetics and trials of pharmacological modulation of the various reactions induced by picryl chloride and oxazolone in Swiss mice provided evidence of differences in behavior between the two agents.
将苦味酸氯涂抹于瑞士小鼠耳部会引发明显的原发性刺激炎症(3至6小时后达到最大值),且在7天前进行接触致敏后会引发迟发型超敏反应。恶唑酮仅产生微弱的原发性刺激反应。在与上述相同条件下进行接触致敏后,恶唑酮引发的免疫反应在激发后3至6小时就已相当显著,通常在24小时后达到最大值。我们试图通过经皮或全身给予各种类型的化合物来改变这四种炎症类型(对苦味酸氯的原发性刺激和迟发型超敏反应,以及对恶唑酮超敏反应的6小时和24小时阶段)。马来酸氯苯那敏、甲基麦角新碱、西咪替丁、色甘酸钠、保泰松和乙酰水杨酸经皮应用后,不同程度地减轻了苦味酸氯引发的原发性刺激和迟发型超敏炎症。甲基麦角新碱是这些药物中唯一局部应用时能明显降低对恶唑酮免疫反应的药物(6小时阶段反应降低)。全身给药后,这些相同的药物对这四种反应均无影响。所测试的两种皮质类固醇(醋酸氢化可的松和地索奈德)均不同程度地减轻了所有炎症,且局部应用时(特别是地索奈德)总是比全身给药更有效。另一方面,抑制所有炎症类型的吲哚美辛全身给药时更有效。对瑞士小鼠中苦味酸氯和恶唑酮引发的各种反应的动力学研究和药理调节试验提供了这两种药剂行为差异的证据。