title: Assessment of the neural defect in a dog with idiopathic megaesophagus.
abstract: In a dog with megaesophagus, we studied the upper (UES) and lower (LES) esophageal sphincter responses to swallowing, the UES response to intraesophageal balloon distension and acid perfusion, the fasting LES, stomach and upper small bowel motor activity, and the LES response to intraesophageal balloon distension. The findings were compared to those in two normal dogs. In normal dogs, balloon distension (10-40 cc) and acid perfusion (0.1-0.4 N HCl) at 5, 10, and 15 cm distal to the UES produced up to 200% and 100% increases in UES pressure, respectively. Fasting LES activity in these dogs was coupled to the cyclical migrating motor complex (MMC) activity of the stomach and intestine, with phase I, random phase II, and phase III employing 40%, 40%, and 20% of cycle time, respectively. Balloon distension (10-40 cc) at 5, 10, and 15 cm proximal to the LES in phases I, II, and III produced 80-100% relaxation of the sphincter. In the dog with megaesophagus: the UES and LES response to swallowing was normal; balloon distension (10-40 cc) in the upper esophagus produced no significant increase (P greater than 0.05) in UES pressure while acid perfusion (0.1-0.4 N HCl) produced a significant but relatively smaller increase (50%) in UES pressures; phase I MMC activity in this dog was absent or very short in duration (less than 5% cycle time), the activity mostly alternating between phases II and III (75-80% and 20% cycle time, respectively); and balloon distension in the distal esophagus (up to 80 cc) induced no observable relaxation (less than 10%) of the LES.
  
  
  CONCLUSIONS
  The normal UES and LES response to swallowing and the presence of cyclical MMC activity in the LES indicates that the efferent neural pathways, at least to these areas, are intact in the dog with megaesophagus. Absence or decreased response of the UES and LES to intraluminal stimuli suggests that at least the afferent component of the reflex neural pathways is faulty in idiopathic megaesophagus. The location of the defect is yet to be determined.
mesh_terms: D000818:Animals; D003679:Deglutition; D004106:Dilatation; D004283:Dog Diseases / Q000503:physiopathology*; D004285:Dogs / Q000502:physiology*; D004931:Esophageal Achalasia / Q000503:physiopathology / Q000662:veterinary*; D004943:Esophagogastric Junction / Q000187:drug effects / Q000294:innervation*; D006851:Hydrochloric Acid / Q000494:pharmacology; D009475:Neurons, Afferent / Q000502:physiology*; D010528:Peristalsis; D011312:Pressure
chemical_list: D006851:Hydrochloric Acid