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2003 Abstract: Electrical Stimulation of the Vagus Nerve in Disordered Esophageal Motility: an Animal Model of Achalasia.
AbstractID – 107029 Presentation Preference – Oral
Resident's Prize – Resident's Prize
Category – Esophageal (S2)  

Electrical Stimulation of the Vagus Nerve in Disordered Esophageal Motility: an Animal Model of Achalasia.

Yashodhan S Khajanchee, Michael J Barra, Roger Van Andel, Paul D Hansen, Lee L Swanstrom, Portland, OR; Albuquerque, NM.

Objective: Esophageal peristalsis generally does not return to normal following surgical treatment of achalasia. Electrical stimulation of the vagus nerve is known to produce antegrade peristalsis in the normal opossum esophagus; however, it is not known whether electrical stimulation will induce return of peristalsis once an achalasia-like disorder has been established. The objective of this study is to see whether electrical stimulation of the vagal nerve can reinstitute antegrade peristalsis in an animal model of achalasia. Method: Fifteen adult opossums (Didelphis virginiana) were divided in to three groups. In Group1 (n=6) a loose Gore-Tex band (110% of the esophageal circumference) was placed around the gastroesophageal junction to prevent relaxation of the lower esophageal sphincter (LES) during swallowing. In Group2 (n=6) a relatively tighter band (90% of the esophageal circumference) was used to further elevate the LES pressure. At six weeks following manometric and radiolologic confirmation of achalasia, electrical stimulation of the esophagus was performed before and after removal of the band using a graduated square wave electrical stimulus. Sham surgery was performed on three animals (Group3). Changes in esophageal neural plexi were assessed histologically. Results: Animals in Group1 demonstrated a vigorous variety of achalasia (high amplitude simultaneous, repetitive contractions), moderate esophageal dilatation, and degeneration of 10%-50% of nerve plexi. In Group2 animals developed amotile achalasia with typical low amplitude simultaneous (mirror image) contractions, severely dilated (bird's beak) esophagus and degeneration of 40% -65% of nerve plexi. Vagal stimulation in Group1 demonstrated a significant increase in the amplitude of contractions (p<0.001), and return of peristaltic activity in 30% of swallows before band removal. After band removal all the contractions were peristaltic. In Group2, vagal stimulation before and after removal of the band demonstrated significant increase in amplitude of contractions (p<0.001) but no return of propagative peristalsis. Conclusion: Electrical stimulation of the vagus nerve improves the force of esophageal contractions irrespective of the severity of the disease; however, peristaltic activity returns back to normal only in vigorous (milder) variety of achalasia. Whether chronic stimulation in case of amotile achalasia will lead to return of normal peristaltic activity needs to be investigated.

 



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