PROTECTION BY ALMAGATE OF ETHANOL-INDUCED GASTRIC-MUCOSAL DAMAGE IN RATS

The study was designed to analyse the protective effects of almagate o n a model of gastric injury, ethanol-induced mucosal damage, in which acid plays little, if any, role. Pretreatment with almagate dose-depen dently reduced the level of gastric damage induced by oral administrat ion of 1 mL 100% ethanol. Administration of 12 mu mol kg(-1) almagate 30 min before ethanol significantly reduced the area of mucosal damage by 65 +/- 10%, and the maximum level of inhibition (74 +/- 11%) was o btained with 150 mu mol kg(-1) almagate. Administration of higher dose s of almagate (200-250 mu mol kg(-1)) did not result in any further in crease in the level of protection against ethanol-induced gastric dama ge. Administration of 1 mL 100% ethanol induces substantial damage to the gastric mucosa, with nearly 40% of the length of the section evalu ated exhibiting deep necrotic and haemorrhagic damage. Pretreatment wi th almagate caused a significant diminution in all parameters of histo logical damage, whereas damage to the epithelial cell layer was only s ignificantly reduced by pretreatment with the highest doses evaluated (25, 50 and 150 mu mol kg(-1)). Administration of aluminium hydroxide did not modify ethanol-induced mucosal damage, even at doses containin g concentrations of aluminium higher than those present in gastroprote ctive doses of almagate. Pretreatment with sucralfate, another alumini um containing compound, at doses of 250 mu mol kg(-1) protected the mu cosa, although lower doses did not. The present study has shown that a lmagate prevents ethanol-induced gastric mucosal damage. This protecti ve effect seems independent of any antacid activity, related to its co ntent in magnesium, and mediated by an increase in gastroprotective pr ostaglandins in the mucosa of the stomach.