Objective: To determine the effect of cigarette smoking on proximal duodenal mucosal bicarbonate secretion, an important defense mechanism against acid and peptic damage.
Design: Prospective study.
Setting: Clinical research laboratory in a university hospital.
Patients: Thirteen healthy adults (7 smokers and 6 nonsmokers) who had no history of peptic ulcer disease.
Interventions: Participants smoked (1 cigarette/15 min during a period of 1 hour, smokers only) or sham smoked (puffing on an unlit cigarette) during duodenal perfusion with saline, hydrochloric acid, or prostaglandin E2 (PGE2).
Measurements: Collection of proximal duodenal secretions using a modified duodenal tube with occluding balloons and quantitation of duodenal mucosal bicarbonate secretion.
Results: During sham smoking both smokers and nonsmokers had comparable basal as well as H+-stimulated and PGE2-stimulated duodenal mucosal bicarbonate secretion. Compared with sham smoking, smoking did not significantly alter basal bicarbonate secretion (201 mol/cm per hour [95% CI, 152 to 250 mol/cm per hour] compared with 178 mol/cm per hour [CI, 134 to 222 mol/cm per hour], respectively). However, compared with sham smoking, smoking markedly reduced (P < 0.01) the increase in duodenal bicarbonate secretion in response to luminal acidification by approximately 80% (from 242 mol/cm per hour [CI, 41 to 443 mol/cm per hour] to 53 mol/cm per hour [CI, 107 to 197 mol/cm per hour]); a decrease was observed in each participant. In contrast, smoking had no significant effect on the response to luminal PGE2.
Conclusions: Cigarette smoking markedly inhibited acid-stimulated human duodenal mucosal bicarbonate secretion. This adverse effect of smoking may, at least in part, explain the role of cigarette smoking in the pathogenesis and natural history of duodenal ulcer disease.