Abstract

Transient lower oesophageal sphincter relaxation (LOSR) is the major mechanism underlying gastro-oesophageal reflux. The mediation and control of LOSRs are incompletely understood but evidence suggests a neural inhibitory mechanism. In this study we have evaluated the effect of gastric distension on LOS function in 16 patients with untreated idiopathic achalasia and compared it with that in 10 healthy controls. With the subjects sitting, the stomach was distended with a liquid mixture that generated 750 ml CO2. Oesophageal pH and motility were monitored for 10 minutes before and after distension. In normal controls, gastric distension induced a four-fold increase in the rate of LOSRs and gas reflux episodes (as evidenced by oesophageal common cavities), whereas this response was absent in the achalasia patients. Basal LOS pressure did not change in either group. These findings are consistent with the notion that transient LOSRs induced by gastric distension are neurally mediated, probably by the same inhibitory nerves that govern swallow mediated LOS relaxation.