IMPAIRMENT OF VAGAL FUNCTION IN REFLUX ESOPHAGITIS

  • 1 January 1985
    • journal article
    • research article
    • Vol. 54  (213) , 61-74
Abstract
Autonomic nervous function in reflux esophagitis was assessed by measuring the response of the lower esophageal sphincter to abdominal compression, gastric secretory response to insulin-induced hypoglycemia and pulse rate variability with respiration. Rise in intra-abdominal pressure normally caused an increase in lower esophageal sphincter pressure through a vagally mediated mechanism. In 59 of 83 patients with reflux esophagitis the sphincter response was subnormal, and this was commoner in older patients but was unrelated to the presence of a hiatal hernia. During esophageal acid perfusion, the onset of pain, but not that of disordered motility, was delayed in those with an abnormal sphincter response suggesting impairment of afferent autonomic function. Efferent gastric vagal function, assessed by the gastric secretory response to insulin induced hypolycemia and expressed as a ratio of the maximal acid output after pentagastrin, was subnormal in 15 of 27 patients with reflux esophagitis. Pulse rate variability with deep respiration, an indicator of one aspect of non-alimentary vagal function, was subnormal in 18 of 62 patients with reflux esophagitis. There was no correlation between abnormalities in these 3 tests of vagal function or with the severity of esophagitis. Vagal impairment is common in reflux esophagitis. As impairment of vagal function is not confined to the alimentary system it is unlikely to be simply a consequence of reflux esophagitis and may be important in the pathogenesis of gastroesophageal reflux.