[Establishment of a novel Bama minipig model of laryngopharyngeal reflux via endoscopic cricopharyngeal myotomy].

To establish a novel laryngopharyngeal reflux model in Bama minipigs excluding concurrent gastroesophageal reflux through endoscopic cricopharyngeal myotomy. Twelve 8-month-old male Bama minipigs were randomly assigned to three groups: Group 1 underwent cricopharyngeal myotomy alone, Group 2 underwent combined cricopharyngeal and lower esophageal sphincter myotomy, and Group 3 served as the control group. Following a one-week acclimatization period, the respective surgical procedures were performed. At 2 weeks postoperatively, laryngopharyngeal pH monitoring was conducted on all pigs. At 8 weeks, histopathological assessment using hematoxylin and eosin (HE) staining, transmission electron microscopy of the laryngopharyngeal mucosa, and quantification of pepsin in the laryngopharyngeal and distal esophageal mucosa were performed to analyze intergroup differences and to elucidate the occurrence and pathologic featuresof LPR. Two weeks postoperatively, experimental groups exhibited laryngopharyngeal reflux episodes with pH<5.0, in contrast to the control group. HE staining at 8 weeks revealed inflammatory changes in the laryngopharyngeal mucosa of Groups 1 and 2, accompanied by increased intercellular spaces and decreased desmosome density under electron microscopy, indicating a pathogenic mechanism involving disruption of intercellular junctions by refluxate. Statistically significant differences in pepsin expression ofthe vocalcords mucosal were observed among groups(=88.427,<0.001).Group 2 exhibited elevated pepsin expression in the distal esophageal mucosa than Groups 1 and 3, suggesting concurrent GERD only occured in Group 2. Endoscopic cricopharyngeal myotomy induces LPRD in Bama minipigs without concurrent GERD by reducing upper esophageal sphincter pressure, thereby offering a model that closely resembles the clinical features of LPRD.