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 (PAW mEq/hr) of hydrochloric acid following a subcutaneous injection of histalog (1.5 mg/kg), and selective H2-stimulation as delta PAO = PAOplacebo-PAOcimetidine. 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 less than 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 less than 0.01). Mean delta 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 less than 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, there is a depression of gastric H2-histamine receptor function.