Nissen fundoplication has a vagolytic effect on the lower esophageal sphincter

Laparoscopic Nissen fundoplication is an increasingly utilized option for the treatment of gastroesophageal reflux disease (GERD). However, many questions remain as to the mechanism by which this operation prevents GERD in those without hiatal hernias or incompetent lower esophageal sphincters (LES). It is known that these patients experience reflux due to excess transient lower esophageal sphincter relaxations (TLESR), inappropriate and short-lived relaxation of the LES and crural diaphragm. The purpose of this study was to determine if Nissen fundoplication affects the neural pathways involved in the TLESR reflex.

Five dogs were anesthetized and intubated. Both vagal nerves and the right phrenic nerve were isolated. A continuous water perfusion manometric catheter was situated at the LES. The nerves were then electrically stimulated and the resultant pressure at the LES measured at baseline, and during and after an open Nissen fundoplication.

The mean LES pressures before dissection, after esophago-gastric mobilization, and after fundoplication were 47 +/- 13 mmHg, 21 +/- 9 mmHg, and 14 +/- 4 mmHg, respectively. All differences were significant. There was no change noted in LES pressure with stimulation of either or both of the phrenic nerves without concomitant vagal stimulation.

Nissen fundoplication may prevent GERD in those without a hiatal hernia or incompetent LES by disrupting the efferent vagal fibers to the LES. Such fibers mediate TLESR which are responsible for GERD in these patients.