Objective: Laryngopharyngeal reflux disease (LPRD) is an inflammatory condition caused by the reflux of gastric contents above the upper esophageal sphincter into areas such as the throat and nasal cavity. Its primary symptoms include hoarseness, a sensation of foreign body in the throat, and chronic cough, however, the specific mechanism remains unclear.This study employed the LPRD animal model to investigate the effects of refluxed material on laryngeal sensory and motor nerves and to explore the underlying mechanisms.
Methods: An endogenous LPRD rat model was established by destroying the gastric His angle, ligating the forestomach along the “limiting ridge” and simultaneously damaging the diaphragm at the esophageal hiatus. The experimental group was divided into three subgroups: the 3-day reflux group, the 7-day reflux group, and the 14-day reflux group. Pharyngeal tissue underwent pepsin immunohistochemical staining to observe rat pharyngeal conditions. Western blot analysis measured expression of the pain-sensing proteins TRPV1 and CGRP in the larynx.Immunofluorescence experiments quantified the effective membrane area of motor nerve endplates in the larynx.
Results: The LPRD model group exhibited positive immunohisto-chemical staining for pepsin in the vocal folds;Immunofluorescence analysis revealed increased free endplate membrane area and reduced neurofilament-endplate membrane connection area in the LPRD model group compared to the control group (P<0.05); Western blot analysis demonstrated significantly higher TRPV1 and CGRP expression in the 3-day reflux group than in the control group (P<0.05), with expression levels decreasing over time.
Conclusions: Through the LPRD model, it was discovered that pharyngeal reflux material may cause sensory and motor abnormalities in the pharynx by affecting TRPV1 and CGRP expression as well as the surface area of motor endplate membranes.