A double-blind study was conducted to compare gastric ulcer healing time in nontreated dogs with that in dogs treated with either cimetidine or omeprazole. Single ulcers were created in the gastric antrum by use of a suction biopsy capsule. Each dog was given 25 mg of aspirin/kg of body weight orally for 20 days after ulcer induction. Five control dogs were given aspirin only (no anti-ulcer medication) during the 20-day study. Six dogs were given cimetidine at dosage of 10 mg/kg orally every 8 hours, and 6 dogs were given omeprazole orally at dosage of 2 micromole/kg (0.7 mg/kg) once daily. All dogs were examined endoscopically on days 5, 10, 15, and 20 and were given a score for the size of the mechanically created ulcer and a score for the degree of aspirin-induced gastritis. All dogs were euthanatized on day 21, and gastric lesions were examined histologically. Significant differences were not evident in ulcer healing scores or degree of aspirin-induced gastritis among treated and nontreated dogs on days 5, 10, 15, and 20. However, aspirin-induced gastritis was less severe in dogs of the omeprazole group than in dogs of the cimetidine or control group on each day observations were made. The effect of omeprazole given once daily was comparable with that of cimetidine given every 8 hours in lessening aspirin-induced gastritis.

OBJECTIVE To evaluate the correlation between the density of native gastric Helicobacter spp and the presence of gastric lesions in dogs. ANIMALS 80 dogs of various breeds, sexes, and ages. PROCEDURES Gastroscopic and histologic examinations were performed for all dogs. Helicobacter spp were detected by combining evaluation of urease activity and results of bacteriologic culture, microscopic observation, and a 16S rRNA PCR assay. The density of Helicobacter-like organisms was evaluated with light microscopy by use of Warthin-Starry modified stain. Correlations were evaluated by use of the Spearman correlation analysis. RESULTS Gastritis was found in 55 of 80 dogs and classified as mild (n = 31), moderate (16), or severe (8). Of these 55 dogs, only 8 had clinical signs. Histologic examination revealed some degree of lymphocytic-plasmacytic infiltrate, mild eosinophilia, and neutrophilic inflammation in the lamina propria. Seventy-six dogs had positive results for Helicobacter spp. Helicobacter pylori DNA was not detected. Low density and homogeneous distribution of Helicobacter spp were observed in all gastric zones. CONCLUSIONS AND CLINICAL RELEVANCE A significant correlation between density of Helicobacter spp and gastroscopic or histologic lesions was not detected. These findings supported the contention that there is no correlation between general Helicobacter spp density or numbers and gastritis in dogs.

Objective: This research work aimed to assess the histopathological features and degree of gas¬tritis severity in a rat model, induced by Helicobacter pylori infection after administering omepra¬zole, amoxicillin, and clarithromycin as the standard first-line eradication regimen. Material and Methods: Twenty-one male rats were adapted for 7 days and randomly divided into three equal groups. Group 1 was considered a negative control. Group 2 and Group 3 were treated as H. pylori-inoculated groups. Group 2 was set as a positive control. Group 3 was admin¬istered omeprazole, amoxicillin, and clarithromycin as a first-line eradication regimen. Gastric histopathological examination was conducted. The difference in the severity of gastritis among the groups was examined using the one-way analysis of variance test. The significance was deter¬mined to be p < 0.05. Results: Gastritis was found in all inoculated groups. The severity of gastritis was highest in Group 2 (p < 0.05). We could see a refinement in gastritis severity after administering omeprazole, amox¬icillin, and clarithromycin as a first-line eradication regimen (Group 3 vs. Group 2; p [J Adv Vet Anim Res 2021; 8(1.000): 158-163]