Influence of the vagus nerve upon the reflex control of the lower oesophageal sphincter.

Abstract

SUMMARY In 24 control patients the lower oesophageal sphincter responded to graded increments in intra-abdominal pressure by a significant and sustained rise in tone. This response was abolished by atropine and was also absent in nine of 11 patients who had previously undergone truncal vagotomy for duodenal ulcer but not in the remaining two who had recurrent ulceration. In six patients studied after proximal gastric vagotomy a variable response was seen. Gastric efferent vagal function was assessed by a combined insulin/pentagastrin gastric secretory test and did not correlate closely with the lower oesophageal sphincteric response to increased intra-gastric pressure. These findings are explicable if it is assumed that truncal vagotomy interrupts the afferent limb of a reflex arc regulating lower oesophageal sphincteric tone.Lower oesophageal sphincter pressure has been shown to increase with a rise in intra-abdominal pressure' 2 and this may represent an important mechanism protecting against gastro-oesophgeal reflux. Whether the vagus nerve is concerned in the reflex control of the lower oesophageal sphincter is uncertain and while some have found that truncal vagotomy abolishes the sphincteric response to increase in intra-abdominal pressure, 3 4 others have failed to do so and have suggested the pressure increase is brought about by diaphragmatic contraction.To investigate the possible role of the vagus in the reflex control of the lower oesophageal sphincter, we have studied the effects of atropine and of truncal and proximal gastric vagotomy upon the response of the lower oesophageal sphincter to increase in intra-abdominal pressure. Methods PATIENTSThe control group consisted of 24 patients (21 men) with a mean age of 43 years (range 30-70 years), who had undergone upper gastrointestinal fibreoptic endoscopy for dyspepsia. Eighteen had chronic

Dysphagia-Gastroesophageal Reflux Complex: Complications Due to Dysfunction of Solitary Tract Nucleus-Mediated Vago-Vagal Reflex

“…These nerve terminals use a set of neurotransmitters for contraction and relaxation of functionally defined LES, e.g., acetylcholine (for contraction) from the parasympathetic vagal nerve, and vasoactive intestinal polypeptide and nitric oxide (for relaxation), and substance P (for contraction) from intrinsic nerve terminals [11,14,22,24]. Mediated by the vagal afferents, the reflex relaxation of LES results from pharyngeal and esophageal distension [1,25], and the reflex contraction of LES results from gastric distension and increased abdominal pressure [20,21,31]. The latter reflex is abnormal in adult patients with GERD and the term "gastroesophageal dyssynergia" is proposed to describe such a pathomechanism of GER [30].…”

Nervous Control of Distension-Induced Relaxation of the Porcine Lower Oesophageal Sphincter

“…a response which has been alleged to be conveyed via the vagus nerve [14][15][16]. Another matter of concern when studying lower oesophageal sphincter func tion is the use of anaesthesia.…”

Esophageal motility

“…This contraction occurs in continuity with the peristaltic wave of the esophageal body and may represent the response of esophageal body-type circular Short-lived increases in LES pressure also occur secondary to increases in intra-abdominal pressure. Considerable controversy exists as to whether this rise in LES pressure is due to reflex contraction or merely due to passive transmission of the increased intraabdominal pressure (47, 154,269,317,349,360,500). The studies that show this to be a true reflex also suggest that it is vagally mediated and dependent on cholinergic neurons (269,315,360).…”