The study was conducted on 20 adult healthy medium-sized mongrel dogs. Injection of dexamethasone @ 1？mg/kg, IV, b.i.d., was administered to create gastric ulcerations and erosions. Thereafter all the animals were randomly divided into 5 equal treatment groups. Animals of groups I, II, III, IV, and V were treated with oral administration of lansoprazole @ 1.5？mg/kg, sucralfate @ 1？g/animal, misoprostol @ 10？μg/kg, famotidine @ 1？mg/kg, and Seabuckthorn seed oil @ 5？mL/animal, twice a day, respectively. Gastroendoscopically, complete healing of GUE lesions was earliest in Seabuckthorn- (SBT-) oil-treated group ( ) followed by famotidine ( ), lansoprazole ( ), misoprostol ( ), and sucralfate ( ), respectively. A marked improvement in appetite was observed in all animals. Melena was continued till day 3 in SBT group, day 6 in lansoprazole- and famotidine-treated animals, and day 9 in sucralfate and misoprostol group animals. Fecal occult blood test was positive in all animals till there was endoscopic evidence of gastric bleeding. Hematological parameters improved markedly towards the end of the study. Serum biochemical parameters remained within normal physiological limits throughout the study. It is concluded that Seabuckthorn oil was the best therapeutic agent for dexamethasone-induced GUE in dogs followed by famotidine, lansoprazole, misoprostol, and sucralfate. 1. Introduction Gastric ulcerations and erosions (GUEs) are a well-known entity in veterinary medicine. The mucosal defect penetrating through the gastric muscularis mucosa is termed as “gastric ulcer,” whereas the superficial ulcer that does not extend far into the mucosa is termed as “gastric erosion.” But in routine clinical practice, it is difficult to differentiate between both conditions by all known diagnostic methods except histopathology. So this complex of gastric ulcerations and erosions is combined termed as GUE. In small animals, it develops mainly due to long-term administration of steroidal and nonsteroidal anti-inflammatory drugs (NSAIDs). Corticosteroids are ulcerogenic in dogs even at therapeutic doses [1]. Ulcerogenic activity of these drugs is attributed to their inhibitory effect on synthesis of prostaglandins, altering the biochemical structure of gastric mucous which increases acid output. This exposes the gastric wall to its own acids leading to GUE. Other potential causes of gastric ulceration in animals include neoplasia like lymphosarcoma, adenocarinomas, gastrinoma (Zollinger-Ellison syndrome), and mastocytosis, systemic diseases like hepatic and renal disease,
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