Influence of caloric labyrinthine stimulation on oesophageal motor function

There is incomplete understanding of the factors regulating smooth muscle primary peristalsis and of the reflux-associated transient lower oesophageal sphincter relaxations which are under postural control and which occur independently of swallowing. We examined the effects of labyrinthine stimulation on basal lower oesophageal sphincter tone, the frequency of non-swallow associated lower oesophageal sphincter relaxation and on the amplitude of primary peristalsis in the distal oesophagus. In 13 healthy volunteers, labyrinthine stimulation was produced by infusion of water at 10°C into the external auditory canal for 5 minutes, or until nausea ensued. A manometric sleeve catheter assembly monitored lower oesophageal sphincter pressure while side holes recorded pharyngeal, mid and lower oesophageal, and gastric pressures. Recordings were made during labyrinthine stimulation and during matched control periods. Caloric stimulation caused a minor but significant fall in mean basal lower oesophageal sphincter pressure of 14% (P = 0.04) and had no detectable effect on oesophageal peristalsis. In association with vomiting induced by labyrinthine stimulation in 3 subjects, lower oesophageal sphincter pressure fell rapidly by 61% (P = 0.03) from control levels and this inhibition persisted for up to 20 minutes after vomiting. For 10 minutes post-emesis, primary peristaltic amplitude was reduced by 50% (P< 0.001). Swallowing triggered a completely propagated peristaltic wave significantly loss often during the post-emetic period. The rate of occurrence of transient lower oesophageal sphincter relaxations was not influenced significantly by labyrinthine stimulation. These findings are consistent with a functionally important role for the brainstem in the control of motor function of the smooth muscleoesophagus but do not permit distinction of a direct effect from a secondary humoral effect as part of the vomiting reflex.