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组胺H1和H2受体在ICR小鼠被动皮肤过敏反应诱导的搔抓行为中的作用

Participation of histamine H1 and H2 receptors in passive cutaneous anaphylaxis-induced scratching behavior in ICR mice.

作者信息

Inagaki N, Nakamura N, Nagao M, Musoh K, Kawasaki H, Nagai H

机构信息

Department of Pharmacology, Gifu Pharmaceutical University, Japan.

出版信息

Eur J Pharmacol. 1999 Feb 19;367(2-3):361-71. doi: 10.1016/s0014-2999(98)00974-1.

DOI:10.1016/s0014-2999(98)00974-1
PMID:10079012
Abstract

Scratching behavior associated with passive cutaneous anaphylaxis was examined and compared to that induced by compound 48/80 or histamine in ICR mice. Elicitation of passive cutaneous anaphylaxis, and intradermal injections of compound 48/80, histamine or serotonin induced both scratching behavior and vascular permeability increase in ICR mice. In mast cell-deficient WBB6F1-W/Wv mice, although histamine induced scratching behavior and vascular permeability increase, passive cutaneous anaphylaxis was not observed. Cetirizine and terfenadine significantly inhibited the scratching behavior and vascular permeability increase caused by passive cutaneous anaphylaxis, compound 48/80 and histamine. The histamine H1 receptor antagonists inhibited the vascular permeability increase almost completely, whereas they failed to abolish the scratching behavior. Famotidine and ranitidine significantly inhibited the scratching behavior caused by histamine. The histamine H2 receptor antagonists did not affect the vascular permeability increase caused by histamine. The combination of cetirizine and ranitidine abolished the histamine-induced scratching behavior. The combination, however, failed to potentiate the inhibition of passive cutaneous anaphylaxis-induced scratching behavior significantly. The results indicated that histamine induces scratching behavior in ICR mice through both histamine H1 and H2 receptors, and that histamine plays a major role in passive cutaneous anaphylaxis-induced scratching behavior. Histamine might also play an important role in compound 48/80-induced scratching behavior.

摘要

对与被动皮肤过敏反应相关的抓挠行为进行了研究,并与ICR小鼠中由化合物48/80或组胺诱导的抓挠行为进行了比较。被动皮肤过敏反应的激发以及化合物48/80、组胺或5-羟色胺的皮内注射均在ICR小鼠中诱导了抓挠行为和血管通透性增加。在肥大细胞缺陷的WBB6F1-W/Wv小鼠中,尽管组胺诱导了抓挠行为和血管通透性增加,但未观察到被动皮肤过敏反应。西替利嗪和特非那定显著抑制了由被动皮肤过敏反应、化合物48/80和组胺引起的抓挠行为和血管通透性增加。组胺H1受体拮抗剂几乎完全抑制了血管通透性增加,然而,它们未能消除抓挠行为。法莫替丁和雷尼替丁显著抑制了组胺引起的抓挠行为。组胺H2受体拮抗剂不影响组胺引起的血管通透性增加。西替利嗪和雷尼替丁的组合消除了组胺诱导的抓挠行为。然而,该组合未能显著增强对被动皮肤过敏反应诱导的抓挠行为的抑制作用。结果表明,组胺通过组胺H1和H2受体在ICR小鼠中诱导抓挠行为,并且组胺在被动皮肤过敏反应诱导的抓挠行为中起主要作用。组胺在化合物48/80诱导的抓挠行为中可能也起重要作用。

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