A Model for Gastric Banding in the Treatment of Morbid Obesity: The Effect of Chronic Partial Gastric Outlet Obstruction on Esophageal Physiology

Laparoscopic gastric banding has become a mainstay of surgical therapy for morbid obesity over the last decade. The first adjustable gastric band device was used in humans in 1986,1 and gastric banding has subsequently become widely used in Europe and Australia. In 2001, the U.S. Food and Drug Administration approved the first adjustable gastric band device for use in humans, and since then, application of gastric banding has increased in frequency in the United States. An important reason for the increasing popularity of gastric banding is that major morbidity and mortality are at least 10-fold less than that associated with gastric bypass and malabsorptive procedures.2,3 Despite these advantages, concerns remain regarding the long-term sequelae of gastric banding. A major concern is the effect of gastric banding on esophageal function. Gastric banding establishes a relative outlet obstruction of the esophagus and proximal stomach, and the long-term effects of such obstruction on esophageal motility and lower esophageal sphincter (LES) function remain unknown. Motility disorders in both animals and humans have been well described following placement of bands at the esophagogastric junction (EGJ).4–10 Esophageal dysmotility has also been noted following gastric banding in humans11,12 but has not been studied on a prospective basis, nor has it been studied in animal models. When esophageal dysmotility does develop, it can be a disabling condition. While rare, it is important to be vigilant for such complications in gastric band patients. Obesity is independently associated with an increased prevalence of abnormal esophageal function,13–16 and is probably an independent risk factor for gastroesophageal reflux disease (GERD) as well.15–19 It is therefore critical to understand the effect of bariatric surgical procedures on esophageal and LES function in this patient population at high risk for esophageal dysfunction in the first place. The North American opossum (Didelphis virginiana) represents an excellent model for the study of human esophageal physiology.19 The opossum foregut is closely analogous to the human foregut with respect to the proportion of smooth and skeletal muscle and intrinsic motor function.20 In addition, the opossum esophagus is large enough to allow for accurate manometric and radiographic evaluation. Normal opossum esophageal motility was characterized by Schulze et al in 1977.20 Subsequently, the opossum model has been used to study esophageal dysmotility in an obstructive model that reproduces the clinical and manometric features of achalasia.4 Khajanchee et al found severe dysmotility culminating in aperistalsis caused by band placement around the esophagogastric junction, effectively preventing receptive relaxation of the LES.4 Whether a functional obstruction immediately distal to the EGJ has the same effect is unknown. This study uses an in vivo opossum model to explore the effects of nonadjustable gastric banding on esophageal and LES function. Our specific aims are to establish an animal model for gastric banding, to identify changes in esophageal and LES function following gastric banding and to assess recoverability of alterations in esophageal function after band removal.