ObjectiveTo develop an experimental model of gastroesophageal reflux-induced esophageal stricture in rats and explore the mechanism of esophageal stricture. MethodsA total of 30 male Sprague-Dawley (SD) rats by random number table method were randomly divided into three groups as follows: an operation+acid perfusion group, first the models of lower esophageal sphincter relaxation and hiatal hernia were made, and then the rats’ esophagus were perfused with hydrochloric acid-pepsin; acid perfusion group, the rats’ esophagus were directly perfused with hydrochloric acid-pepsin; and control group, rats’ esophagus were perfused with normal saline. After 4 weeks of continuous perfusion, the esophageal mucosal injury of SD rats in each group were observed, and the concentrations of inflammatory cytokines [tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-18] in esophageal tissues were detected by enzyme-linked immunosorbent assay. ResultsIn the operation+acid perfusion group, esophageal stricture was formed in 2 SD rats, but no esophageal stenosis was found in the acid perfusion group and the control group. The body weight of rats in the operation+acid perfusion group and the acid perfusion group were lower than that in the control group (P<0.05). The esophageal mucosal injury scores of rats in the operation+acid perfusion group and the acid perfusion group were higher than that in the control group (P<0.001), and the operation+acid perfusion group was higher than that in the acid perfusion group (P=0.014). The concentrations of TNF-α, IL-1β and IL-18 in esophageal tissues were higher in the operation+acid perfusion group and the acid perfusion group than that in the control group (P<0.001), and the operation+acid perfusion group was higher than that in the acid perfusion group (P<0.001). ConclusionsThe anti-reflux barrier is an important part of preventing gastroesophageal reflux disease. The destruction of anti-reflux barrier, hydrochloric acid-pepsin perfusion and inflammatory cytokines jointly induced esophageal inflammation and injury, and even caused esophageal stricture.