Ebrotidine is an H receptor antagonist with gastroprotective activity against ethanol-, aspirin- or stress-induced gastric mucosal damage.

Microcirculatory disturbances of the stomach are thought to be one of the factors contributing to the development of gastric mucosal damages.

Endothelin induced gastric mucosal damage was carried out as described below.

These results could suggest a prominent role of tissue type plasminogen activator in the pathogenesis of endothelin induced gastric mucosal damage.

These reports suggested that inhibition of prostaglandin synthesis was unlikely to be sole mechanism responsible for the gastric damage induced by indomethacin.

The extent of the gastric damage was expressed as the total area ((mm) of haemorrhagic erosion.

Dietary replacement of arachidonic acid by eicosapentaenoic acid results in an enhanced resistance to ethanol induced gastric damage.

An advantage of acemetacin is that it reduces gastric damage when compared to indometacin.

Cytoprotective effect of S-adenosylmethionine compared with that of misoprostol against ethanol-, aspirin-, and stress-induced gastric damage.

Gastric mucosal restitution is an alteration in the morphology/organization of cells in response to gastric damage.