Effect of general anaesthesia on transient lower oesophageal sphincter relaxations in the dog

This report investigates the hypothesis that gastro-oesophageal flow is modulated by central nervous activity. The hypothesis was examined using the canine model in which gastro-oesophageal flow was stimulated by gastric insufflation of air at 80 ml/min and central nervous depression was produced with the anaesthetic agents thiopentone, nitrous oxide and halothane. Duplicate paired studies were performed in four dogs, either unsedated or anaesthetized. Gastro-oesophageal flow was assessed manometrically by a sleeve catheter assembly and by pH electrode. Gastric compliance was assessed by inflation of a thin-walled, plastic bag. Transient lower oesophageal sphincter relaxation, the dominant mechanism of retrograde trans-sphincter flow in unsedated animals, was abolished by general anaesthesia. Retrograde flow of gas across the lower oesophageal sphincter in anaesthetized animals eventually occurred, but only after massive gastric distension and elevation of gastric pressure to lower oesophageal sphincter pressure. The effects observed could not be explained by a direct action of anaesthetic on the lower oesophageal sphincter or on the gastric wall. It is proposed that general anaesthesia results in blockade of the neural pathway responsible for transient lower oesophageal sphincter relaxation by withdrawal of facilitative higher centre activity. The findings have implications for the use of sedation in experimental studies on factors which control gastro-oesophageal reflux, and clinical application to the risk of tracheal aspiration during general anaesthesia.