Abstract
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.
| Original language | English |
|---|---|
| Pages (from-to) | 491-496 |
| Number of pages | 6 |
| Journal | Chest |
| Volume | 89 |
| Issue number | 4 |
| State | Published - Jan 1 1986 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Pulmonary and Respiratory Medicine
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Suppression of gastric H2-receptor mediated function in patients with bronchial asthma and ragweed allergy. / Gonzalez, H.; Ahmed, T.
In: Chest, Vol. 89, No. 4, 01.01.1986, p. 491-496.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Suppression of gastric H2-receptor mediated function in patients with bronchial asthma and ragweed allergy
AU - Gonzalez, H.
AU - Ahmed, T.
PY - 1986/1/1
Y1 - 1986/1/1
N2 - 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.
AB - 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.
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M3 - Article
VL - 89
SP - 491
EP - 496
JO - Chest
JF - Chest
SN - 0012-3692
IS - 4
ER -