Grönneberg R, Zetterström O
Department of Lung Medicine, Huddinge University Hospital, Sweden.
Clin Exp Allergy. 1992 Feb;22(2):257-63. doi: 10.1111/j.1365-2222.1992.tb03081.x.
The capacity of the beta 2-agonist terbutaline and the longer-acting beta 2-agonist formoterol to suppress the development of late phase skin reactions to anti-human IgE was evaluated in 17 healthy volunteers. Anti-IgE injected intradermally per se induced an early weal and flare reaction, followed by a progressively increasing induration, the LCR, with a duration of greater than or equal to 24 hr. The LCR was inhibited by 40% when the weal was infiltrated with formoterol 250 ng 30 min after challenge (n = 9, P less than 0.01). The same anti-LCR effect was achieved by compensating for the shorter duration of action of terbutaline with repeated drug infiltration in 12.5 micrograms doses of the weal produced by anti-IgE up to 3 1/2 hr after challenge (n = 8). The data support the hypothesis that beta 2-agonists, both short- and long-acting, inhibit IgE-dependent LCRs by preferentially interacting with inflammatory events after the initial mast cell degranulation.
在17名健康志愿者中评估了β2-激动剂特布他林和长效β2-激动剂福莫特罗抑制抗人IgE所致皮肤迟发相反应发展的能力。皮内注射抗IgE本身可诱发早期风团和潮红反应，随后硬结逐渐增大，即迟发相反应（LCR），持续时间大于或等于24小时。激发后30分钟，当用250 ng福莫特罗浸润风团时，LCR受到40%的抑制（n = 9，P < 0.01）。在激发后长达3.5小时，通过用12.5微克剂量的特布他林反复浸润抗IgE产生的风团来弥补其作用持续时间较短的问题，可获得相同的抗LCR效果（n = 8）。数据支持这样的假设，即短效和长效β2-激动剂通过在初始肥大细胞脱颗粒后优先与炎症事件相互作用来抑制IgE依赖性LCR。
