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IgE-mediated histamine release was studied using the method of passive peritoneal anaphylaxis (PPA) in the rat. Some β-adrenergic stimulants markedly inhibited this reaction in vivo, the order of potency (ED₅₀μg/kg i. v.) of agents tested being fenoterol (6), salbutamol (40) and isoproterenol (94). Higher activity against the simultaneously measured dye extravasation suggested a dual effect of the drugs on both the cellular (inhibition of histamine release) and the vascular level. The order of potency in modifying vascular injury was, however, reversed, isoproterenol and not fenoterol being relatively more active here, as could be shown by further experiments. Inhibition of histamine release is discussed with respect to (a) methodical requirements and (b) the suggestion that β₂-receptor stimulants (fenoterol, salbutamol) are more selective than isoproterenol.

The action of the two β-stimulants fenoterol and SOM 1122 (α-[[[3-(1-benzimidazolyl)-1,1-dimethylpropyl]amino]methyl]-2-fluoro-4-hydroxybenzyl alcohol methane sulfonate) against inflammatory correlates of bronchial asthma was investigated by performing the following experiments: Passively sensitized guinea pigs were challenged by antigen aerosol under protection of mepyramine. The animal response was a 5- to 6-fold increase in the number of eosinophils in the bronchoalveolar lavage fluid after 1 or 2 days. In addition, increased microvascular permeability was elicited in guinea pig lungs after inhalation of a low concentration of histamine for 60 min. Both inflammatory reactions were inhibited by inhalation of remarkably low concentrations (0.004–0.04%) of the two β-stimulants. These concentrations were 5 to 75 times lower than the EC₅₀ values required for inhibition of acetylcholine-induced bronchoconstriction in the same species. The lung eosinophilia was not modified by inhibitors of lipoxygenase or cyclo-oxygenase.

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