Impairment of vagal function in reflux oesophagitis

Abstract

Autonomic nervous function in reflux oesophagitis was assessed by measuring the response of the lower oesophageal sphincter to abdominal compression, gastric secretory response to insulin-induced hypoglycaemia and pulse rate variability with respiration. Rise in intra-abdominal pressure normally causes an increase in lower oesophageal sphincter pressure through a vagally mediated mechanism. In 59 of 83 patients with reflux oesophagitis the sphincter response was subnormal, and this was commoner in older patients but was unrelated to the presence of a hiatal hernia. During oesophageal 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 hypoglycaemia and expressed as a ratio of the maximal acid output after pentagastrin, was subnormal in 15 of 27 patients with reflux oesophagitis. 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 oesophagitis. There was no correlation between abnormalities in these three tests of vagal function or with the severity of oesophagitis. These findings suggest that vagal impairment is common in reflux oesophagitis. As impairment of vagal function is not confined to the alimentary system it is unlikely to be simply a consequence of reflux oesophagitis and may be important in the pathogenesis of gastro-oesophageal reflux.