Abstract

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.

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