A model for gastric banding in the treatment of morbid obesity: The effect of chronic partial gastric outlet obstruction on esophageal physiology

OBJECTIVE: This work establishes an animal model for nonadjustable gastric banding and characterizes the effect of gastric banding on esophageal physiology. SUMMARY BACKGROUND DATA: Obstruction at the esophagogastric junction (EGJ) results in esophageal dilation and aperistalsis. Although laparoscopic gastric banding as a primary treatment of morbid obesity has been widely accepted, the effects of this therapy on esophageal function remain unknown. METHODS: Twenty-five opossums were randomly divided into sham (n = 5), EGJ band (n = 5), and gastric band (n = 15) groups. Gastric and EGJ bands were surgically placed, and esophageal manometry was performed prebanding, at 2-week intervals during the banding period (up to 14 weeks), and 2 and 4 weeks after band removal. RESULTS: Manometric measures were equivalent prior to banding in all groups. There were no changes in LES or esophageal pressures during the study period in the sham group. During banding, there was a 36% decrease in baseline mean resting lower esophageal sphincter pressure in the gastric band group (P = 0.003). Mean distal esophageal peristaltic pressure decreased from baseline by 36% in gastric band animals (P < 0.001). The incidence of esophageal motility disorder during the study period for sham, EGJ band, and gastric band groups, was 2.9%, 42.1%, and 31.3%, respectively (P = 0.001, P = 0.381, pairwise comparisons of gastric band vs. sham and gastric band versus EGJ groups, respectively). Immediately prior to band removal, the probability of an abnormal peristaltic sequence with each swallow was 1%, 38%, and 16% for sham, EGJ, and gastric band groups, respectively (P < 0.005, pairwise comparisons of band groups with sham). CONCLUSIONS: Nonadjustable gastric banding results in impaired esophageal body motility, a reduction in esophageal peristaltic pressure, and a reduction in resting lower esophageal sphincter pressure. These findings suggest that gastric banding causes esophageal outlet obstruction and subsequent decompensation of peristaltic function as well as a compromise of the native antireflux mechanism.