Bronchial reactivity after Cimetidine treatment was evaluated by the histamine provocation test in 24 patients with atopic bronchial asthma and 10 patients with peptic ulcer. Anti-IgE induced histamine release from isolated basophils was also investigated. After blockade of H2 receptors, an increase of bronchial reactivity and an exacerbation of clinical symptoms were observed in 4 asthmatic patients [17%]. A moderate increase in bronchial reactivity without exacerbation of asthma symptoms was observed in 16 other patients [66%]. In some of the patients treated with Cimetidine an enhancement of IgE-induced histamine release from isolated basophils was observed.

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The effect of drugs applied in the treatment of allergic diseases such as hydrocortisone and disodium cromoglycate-Intal on the release of histamine during immediate allergic response was investigated. Experiments carried out on guinea-pigs showed that after hydrocortisone administration the blood histamine level fell, whereas the histamine concentration in the lung tissue varied, depending on the time of the drug administration in relation to the antigen challenge. Disodium cromoglycate give before induction of an asthma attack in guinea-pigs lowered the histamine level in the blood and in the lung tissue homogenates. Investigations were also carried out on isolated rat mast cells and human basophils. The stabilizing effect of hydrocortisone was much weaker than that of disodium cromoglycate especially regarding mastocytes. It was found that the extent of histamine release from mastocytes and basophils depends on the concentration of the drugs applied and on the type of antigen used for induction of cell degranulation.

Anti-IgE- and antigen-induced histamine release from basophils isolated from 20 atopic patients sensitive to grass pollen allergens was evaluated. The studies were made before and after short-term immunotherapy with Pollinex. It was shown, that after hyposensitization a significant decrease on anti-IgE and specific antigen-induced histamine release from basophils occurs.

The aim of the present study was to evaluate lung function and bronchial reactivity during therapy with the H2-blockers, cimetidine and ranitidine, in order to determine the role of H2-receptors in the bronchial response of asthmatic patients. Bronchial reactivity was evaluated by the histamine provocation test before, and 3 or 6 days after administration of cimetidine (800 mg per day) or ranitidine (300 mg per day). It was shown that after 6 days treatment, an increase in bronchial reactivity occurred in 85% of the patients treated with cimetidine and in 64% of the patients treated with ranitidine. These results seem to confirm the presence of H2 receptors in the bronchial tree of asthmatic patients. Blockade of these receptors causes an increase in bronchial reactivity and potential exacerbation of the asthmatic symptoms.