AIM: To explore the pathological findings in the entire esophagus in rats with reflux esophagitis, and the effects of ecabet sodium (ES). METHODS: A rat model of chronic acid reflux esophagitis was used. In the treatment group, ES was administered after surgery (n = 16). No drug was administered postoperatively to the esophagitis group (n = 9). Sham-operated rats were used as a control group (n = 5). Rats were sacrificed on day 7 after the operation. The epithelial thickness and leukocyte infiltration were examined in the upper, middle and lower areas of the esophagus. The survival rate, incidence of esophageal ulcer, and mean surface area and number of esophageal ulcers were determined in the esophagitis and ES groups. Esophageal histology was assessed in all three groups. RESULTS: Leukocyte infiltration in the esophagitis group was 26.3 +/- 22.0 in the middle esophagus and 8.2 +/- 4.9 in the upper esophagus, which was significantly greater than that in the controls (1.3 +/- 1.1 and 1.4 +/- 1.0, respectively) (P < 0.05). The thickness of the epithelium in the esophagitis group was 210.8 +/- 47.7 microm in the lower esophagus and 204.2 +/- 60.1 microm in the middle esophagus, which was significantly greater than that in the controls (26.0 +/- 5.5 and 21.0 +/- 6.5 microm, respectively) (P < 0.05). The mean number of ulcers per animal in the ES group in the entire esophagus was 5.4 +/- 2.5, which was significantly less than that in the esophagitis group (9.0 +/- 3.5) (P < 0.05). The epithelial thickness in the ES group was 97.5 +/- 32.2 microm in the lower esophagus, which was decreased compared with that in the esophagitis group (210.8 +/- 47.7 microm) (P < 0.05). CONCLUSION: Mucosal inflammation extended to the upper esophagus close to the hypopharynx. Our study suggested that ES may have a useful defensive role in reflux esophagitis.
AIM: To explore the pathological findings in the entire esophagus in rats with reflux esophagitis, and the effects of ecabet sodium (ES). METHODS: A rat model of chronic acid reflux esophagitis was used. In the treatment group, ES was administered after surgery (n = 16). No drug was administered postoperatively to the esophagitis group (n = 9). Sham-operated rats were used as a control group (n = 5). Rats were sacrificed on day 7 after the operation. The epithelial thickness and leukocyte infiltration were examined in the upper, middle and lower areas of the esophagus. The survival rate, incidence of esophageal ulcer, and mean surface area and number of esophageal ulcers were determined in the esophagitis and ES groups. Esophageal histology was assessed in all three groups. RESULTS: Leukocyte infiltration in the esophagitis group was 26.3 +/- 22.0 in the middle esophagus and 8.2 +/- 4.9 in the upper esophagus, which was significantly greater than that in the controls (1.3 +/- 1.1 and 1.4 +/- 1.0, respectively) (P < 0.05). The thickness of the epithelium in the esophagitis group was 210.8 +/- 47.7 microm in the lower esophagus and 204.2 +/- 60.1 microm in the middle esophagus, which was significantly greater than that in the controls (26.0 +/- 5.5 and 21.0 +/- 6.5 microm, respectively) (P < 0.05). The mean number of ulcers per animal in the ES group in the entire esophagus was 5.4 +/- 2.5, which was significantly less than that in the esophagitis group (9.0 +/- 3.5) (P < 0.05). The epithelial thickness in the ES group was 97.5 +/- 32.2 microm in the lower esophagus, which was decreased compared with that in the esophagitis group (210.8 +/- 47.7 microm) (P < 0.05). CONCLUSION:Mucosal inflammation extended to the upper esophagus close to the hypopharynx. Our study suggested that ES may have a useful defensive role in reflux esophagitis.