Suppression of gastric H₂-receptor mediated function in patients with bronchial asthma and ragweed allergy

We have previously demonstrated a depression of airway, vascular, and cutaneous H₂-histamine receptor function in sheep with experimental allergic asthma. In the present investigation, we wished to determine if there is a depression of gastric H₂-receptor function in subjects with allergic bronchial asthma. In eight normal subjects and seven subjects with allergic bronchial asthma and bronchial reactivity to ragweed antigen, gastric H₂-receptor function was assessed by measuring basal and maximal stimulated acid output following pretreatment with a placebo or the H₂-antagonist, cimetidine. Maximal stimulated acid output was defined as the peak acid output (PAO mEq/hr) of hydrochloric acid following a subcutaneous injection of histalog (1.5 mg/kg), and selective H₂-stimulation as Δ PAO = PAO(placebo) - PAO(cimetidine). While basal acid output was not different between the two groups, mean (±SD) PAO was significantly lower in the asthmatic group (14.0 ± 8.2 mEq/hr) than the normal group (27.9 ± 9.4 mEq/hr) (p < 0.01). Mean PAO expressed as percent of predicted maximum was 112 ± 36 percent in the normal group and 61 ± 34 percent in the asthmatic group (p < 0.01). Mean Δ PAO was significantly higher in the normal group (17.1 ± 4.8 mEq/hr) than in the asthmatic group (7.0 ± 5.3 mEq/hr) (p < 0.005) indicating suppressed selective H₂-receptor stimulation in the latter. We conclude that in subjects with bronchial asthma and marked bronchial hyperreactivity to ragweed antigen, antigen, there is a depression of gastric H₂-histamine receptor function.