血小板活化因子诱导的即时和晚期皮肤反应。

J P Rihoux, R Fadel, L Juhlin
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引用次数: 6

摘要

在特应性受试者中,皮内注射血小板活化因子(PAF) 40和400ng,可立即被西替利嗪(10mg,每日两次)明显阻断水肿反应。通过皮肤窗口技术,在2、4、8和24小时,PAF刺激也诱导了显著的嗜酸性粒细胞积累。西替利嗪显著抑制了这种炎症现象。慢性荨麻疹患者,PAF, 100微克皮内注射,诱导即时和晚期皮肤反应(LCR)也阻断西替利嗪,10毫克,一天两次。这些LCR伴有真皮深层被脱颗粒的嗜酸性粒细胞浸润。讨论了paf诱发皮肤反应的病理生理机制以及西替利嗪的作用机制。
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Platelet-activating factor-induced immediate and late cutaneous reactions.

In atopic subjects, intradermal injection of platelet-activating factor (PAF), 40 and 400 ng, resulted in an immediate edema reaction markedly blocked by cetirizine, 10 mg twice a day. PAF challenge also induced a significant eosinophil accumulation evidenced by a skin window technique at 2, 4, 8 and 24 h. This inflammatory phenomenon was significantly inhibited by cetirizine. In patients with chronic urticaria, PAF, 100 micrograms intradermally, induced immediate and late cutaneous reactions (LCR) also blocked by cetirizine, 10 mg twice a day. These LCR were accompanied by an infiltration of the deep dermis by degranulated eosinophils. The pathophysiological mechanism of the PAF-induced skin reactions is discussed as well as the mechanism of action of cetirizine.

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