OBJECTIVES: To examine the integrity of the vagal efferent innervation to the esophagus and to assess esophageal motor performance in dogs with congenital idiopathic megaesophagus. DESIGN: An acute experimental protocol performed in control dogs and dogs with naturally acquired congenital idiopathic megaesophagus under pentobarbitone anesthesia. ANIMALS: 4 dogs with congenital idiopathic megaesophagus and 16 control dogs. PROCEDURE: Esophageal motor nerve conduction studies were performed by recording evoked compound motor action potentials from the tunica muscularis of the distal thoracic portion of the esophagus in response to supramaximal stimulation of the cervical portion of the vagus nerve at cranial and caudal sites. Subsequently, esophageal motor performance was measured over a wide range of esophageal muscle lengths by recording intraesophageal pressure responses to supramaximal twitch and tetanic stimulation of the cervical portion of the vagus at varying, stepwise amounts of esophageal distention. RESULTS: In dogs with congenital idiopathic megaesophagus, no electrophysiologic evidence was found for segmental demyelination or axonal degeneration in cervical vagal motor fibers innervating striated muscle of the thoracic esophagus portion. Nor was spontaneous EMG activity, indicative of esophageal muscle denervation or a primary myopathy, observed. In contrast, esophageal motor performance, which was dependent on esophageal dimensions, was reduced in dogs with congenital idiopathic megaesophagus. CONCLUSIONS: In dogs with congenital idiopathic megaesophagus, the vagal efferent innervation to the esophagus is likely to be normal, a primary esophageal myopathy is unlikely to be present, and the observed reduction in esophageal motor performance may arise as a secondary consequence of altered esophageal biomechanical properties rather than from a primary neuromuscular abnormality.
OBJECTIVES: To examine the integrity of the vagal efferent innervation to the esophagus and to assess esophageal motor performance in dogs with congenital idiopathic megaesophagus. DESIGN: An acute experimental protocol performed in control dogs and dogs with naturally acquired congenital idiopathic megaesophagus under pentobarbitone anesthesia. ANIMALS: 4 dogs with congenital idiopathic megaesophagus and 16 control dogs. PROCEDURE: Esophageal motor nerve conduction studies were performed by recording evoked compound motor action potentials from the tunica muscularis of the distal thoracic portion of the esophagus in response to supramaximal stimulation of the cervical portion of the vagus nerve at cranial and caudal sites. Subsequently, esophageal motor performance was measured over a wide range of esophageal muscle lengths by recording intraesophageal pressure responses to supramaximal twitch and tetanic stimulation of the cervical portion of the vagus at varying, stepwise amounts of esophageal distention. RESULTS: In dogs with congenital idiopathic megaesophagus, no electrophysiologic evidence was found for segmental demyelination or axonal degeneration in cervical vagal motor fibers innervating striated muscle of the thoracic esophagus portion. Nor was spontaneous EMG activity, indicative of esophageal muscle denervation or a primary myopathy, observed. In contrast, esophageal motor performance, which was dependent on esophageal dimensions, was reduced in dogs with congenital idiopathic megaesophagus. CONCLUSIONS: In dogs with congenital idiopathic megaesophagus, the vagal efferent innervation to the esophagus is likely to be normal, a primary esophageal myopathy is unlikely to be present, and the observed reduction in esophageal motor performance may arise as a secondary consequence of altered esophageal biomechanical properties rather than from a primary neuromuscular abnormality.