Cigarette Smoking Inhibits Acid-stimulated Duodenal Mucosal Bicarbonate Secretion

1 November 1993 | Volume 119 Issue 9 | Pages 882-886

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 either 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 µmol/cm per hour [95% CI, 152 to 250 µmol/cm per hour] compared with 178 µmol/cm per hour [CI, 134 to 222 µmol/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 µmol/cm per hour [CI, 41 to 443 µmol/cm per hour] to 53 µmol/cm per hour [CI, –107 to 197 µmol/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.

Author and Article Information

From the University of California at San Diego Medical Center, California, and Odense University Hospital, Denmark.
Requests for Reprints: Jon I. Isenberg, MD, Division of Gastroenterology, Department of Medicine, UCSD Medical Center, 225 Dickinson Street, San Diego, CA 92103-8413.
Acknowledgments: The authors thank Dr. Mark Feldman for his comments on the manuscript. The authors also thank the late Dr. A. Robert (Upjohn; Kalamazoo, Michigan) for the gift of natural PGE₂.
Grant Support: By National Institutes of Health grant AM 33491 and by Forskerakademiet (Denmark).