CIGARETTE-SMOKING INHIBITS ACID-STIMULATED DUODENAL MUCOSAL BICARBONATE SECRETION

Objective: To determine the effect of cigarette smoking on proximal du odenal mucosal bicarbonate secretion, an important defense mechanism a gainst acid and peptic damage. Design: Prospective study. Setting: Cli nical research laboratory in a university hospital. Patients: Thirteen healthy adults (7 smokers and 6 nonsmokers) who had no history of pep tic ulcer disease. Interventions: Participants smoked (1 cigarette/15 min during a period of 1 hour, smokers only) or sham smoked (puffing o n an unlit cigarette) during duodenal perfusion with either saline, hy drochloric acid, or prostaglandin E2 (PGE2). Measurements: Collection of proximal duodenal secretions using a modified duodenal tube with oc cluding balloons and quantitation of duodenal mucosal bicarbonate secr etion. Results: During sham smoking both smokers and nonsmokers had co mparable basal as well as H+-stimulated and PGE2-stimulated duodenal m ucosal bicarbonate secretion. Compared with sham smoking, smoking did not significantly alter basal bicarbonate secretion (201 mumol/cm per hour [95% CI, 152 to 250 mumol/cm per hour] compared with 178 mumol/cm per hour [CI, 134 to 222 mumol/cm per hour], respectively). However, compared with sham smoking, smoking markedly reduced (P < 0.01) the in crease in duodenal bicarbonate secretion in response to luminal acidif ication by approximately 80% (from 242 mumol/cm per hour [CI, 41 to 44 3 mumol/cm per hour] to 53 mumol/cm per hour [CI, -107 to 197 mumol/cm per hour]); a decrease was observed in each participant. In contrast, smoking had no significant effect on the response to luminal PGE2. Co nclusions. 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 p athogenesis and natural history of duodenal ulcer disease.