Effect of vanadium on acute gastric mucosal ulcers induced by indomethacin and ethanol

Gastric mucosal ulcer is a kind of digestive disease, put a person in critical situation if left untreated in a early diagnosis. One of the most side effects of NSAID’s is gastrointestinal upset and gastric ulceration. Ethanol is an agent that proposed to be able to induce gastric ulcers by its ability to release of leukotrienes from mucosa and contraction of submucosal venules. Vanadium is a kind of micronutrient that is effective on many of mechanisms involved in ulceration and acid secretion. The purpose of this study, was to check the effect of vanadate on indomethacin and ethanol induced gastric ulcers in the rat. 72 Sprague Dawley male rats weighing 180 – 120 g in 8 groups (9 in each group) were tested. Sodium metavanadate and indomethacin (Merck, Germany) were resolved in saline NaCl 0.9% made of pure NaCl and deionized water. Indomethacin was prepared from a solution 30 mg / kg. Sodium metavanadate was prepared in 3 dose, 2,5 and 10 mg / kg. Subcutaneous administration of indomethacin, intraperitoneal administration of sodium metavanadate and intragastric administration of alcohol (60 degrees,1 ml)(Merck, Germany) were used. In the first group, animals had received indomethacin 30 mg/kg had wounds with moderate intensity. In comparison with control, groups 2 and 4 showed non significant healing (sodium Metavanadate 2 mg/kg and 10mg/kg). In the second group, the animals that had received ethanol and 5 and 10 mg vanadate,vanadate was able to prevent the injury by ethanol significantly. Vanadate administered i. p. couldn’t protect stomach against indo–ulceration completely, whereas was able to inhibit ulceration by ethanol. It may be concluded that this preventive effect, arise from ability of vanadate to inhibit acid secretion and vascular constriction and leukotrienes release from mucosa, and activity of PMN’s too.