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抗组胺药对人抗IgE诱导的速发和迟发性皮肤过敏反应的影响。

Effect in man of anti-allergic drugs on the immediate and late phase cutaneous allergic reactions induced by anti-IgE.

作者信息

Grönneberg R, Strandberg K, Stålenheim G, Zetterström O

出版信息

Allergy. 1981 Apr;36(3):201-8. doi: 10.1111/j.1398-9995.1981.tb01835.x.

Abstract

Wheal and flare reactions as well as a late cutaneous allergic reaction (LCAR) were induced by anti-human IgE in healthy subjects. The effect of the beta 2-adrenoceptor stimulant terbutaline, the histamine-1 (H1) receptor blocking agent mepyramine and the synthetic glucocorticoid betamethasone on these reactions was studied. All administrations were given intradermally (i.d.). The immediate reaction to anti-IgE was inhibited by 3 micrograms terbutaline and 30 micrograms mepyramine (P less than 0.01) whereas 50 micrograms betamethasone had no effects. Terbutaline had no effect on the flare response induced by i.d. injected histamine but a slight effect on whealing. Terbutaline and mepyramine weakly reduced the LCAR throughout the observation period of 24 h (P less than 0.01). In contrast, betamethasone almost completely abolished the LCAR. It is concluded that the two phases of the skin reaction to anti-IgE are interrelated since an inhibition of the early phase was followed by an attenuation of the LCAR. The mechanism of action of steroids seems to differ fundamentally from that of other anti-allergic drugs since inhibition of the early step in the reaction is not essential to the action on the late step. It is further suggested that terbutaline inhibits anti-IgE-mediated cutaneous reactions by inhibition of the mast cell release reaction.

摘要

在健康受试者中,抗人IgE可诱发风团和潮红反应以及迟发性皮肤过敏反应(LCAR)。研究了β2 - 肾上腺素能受体激动剂特布他林、组胺 - 1(H1)受体阻断剂美吡拉敏和合成糖皮质激素倍他米松对这些反应的影响。所有药物均采用皮内注射(i.d.)。3微克特布他林和30微克美吡拉敏可抑制对抗IgE的即刻反应(P < 0.01),而50微克倍他米松则无作用。特布他林对皮内注射组胺诱发的潮红反应无作用,但对风团有轻微作用。在24小时的观察期内,特布他林和美吡拉敏可轻度降低LCAR(P < 0.01)。相比之下,倍他米松几乎完全消除了LCAR。结论是,皮肤对抗IgE反应的两个阶段相互关联,因为早期阶段的抑制随后伴随着LCAR的减弱。类固醇的作用机制似乎与其他抗过敏药物有根本不同,因为反应早期步骤的抑制对后期步骤的作用并非必不可少。进一步表明,特布他林通过抑制肥大细胞释放反应来抑制抗IgE介导的皮肤反应。

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