We have reviewed the neurobiology of stress ulcers from animal models to potential pharmacotherapeutic mechanisms. The evidence strongly supports the hypothesis that certain stress-related gastric lesions are 'brain-driven' events which may be more effectively managed through central manipulations than by altering local, gastric factors. Recent advances in the use of anxiolytic and antidepressant drugs in the management of stress-related gastric mucosal injury further supports the contention that a brain-gut axis, which may have nervous, peptidergic and classic monoaminergic components, modulates the intricate and complicated pattern of communication between the brain and the stomach. Delineation of the precise pathways which make up this communication as well as their manipulation by various pharmacological agents will be the focus of future research endeavour.

The bile salts of ursodeoxycholic acid, glycoursodeoxycholic acid, tauroursodeoxycholic acid, chenodeoxycholic acid, glycochenodeoxycholic acid, and taurochenodeoxycholic acid were each found to inhibit pepsin proteolytic activity in vitro at various concentrations against the refined substrate n-APDT. The sodium salt of ursodeoxycholic acid was the most potent pepsin inhibitor among those tested.

The morphology of the normal oxyntic mucosa is described. Different animal models for the production of gastric ulcers are briefly reviewed. In a series of rats, wounds were produced by cauterisation of the oxyntic mucosa. The mucosal regeneration process was then followed by morphometrical methods using light and electron microscopy. In particular, the regeneration of the acid-producing parietal cells was followed. Initially, the ulcer area is covered by primitive epithelial cells originating from the mucosa in the wound margin. These cells form the new gastric glands. With time, all specialised epithelial cell types which normally occur in the oxyntic mucosa can be recognised and, if regeneration is allowed to continue, the structure and function of these cells will normalise. However, the amount of glands and the number of parietal cells within the glands remain subnormal.