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Suppression of Gastric H2-Receptor Mediated Function in Patients with Bronchial Asthma and Ragweed Allergy

1986; Elsevier BV; Volume: 89; Issue: 4 Linguagem: Inglês

10.1378/chest.89.4.491

1931-3543

Hugo Gonzalez, Tahir Ahmed,

Respiratory and Cough-Related Research

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 ∆ 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<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 A 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, there is a depression of gastric H2-histamine receptor function. 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 ∆ 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<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 A 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, there is a depression of gastric H2-histamine receptor function.