[The adaptation-protective effect of corticosteroids on the rat gastric mucosa and its mechanism]

The influence of stress-induced corticosteroid production on gastric ulceration, blood flow velocity in gastric microvessels and blood pressure was studied in rats. The role of plasma corticosteroids was investigated by means of blockade of the pituitary-adrenocortical system (PACS) and following corticosterone replacement therapy (400 mu/100 g b.w.). The blockade which was induced by Fi. hydrocortisone administration (7 days before stress, 30 mg/100 g b. w.) resulted in an insufficient corticosteroid production. To evaluate the influence of corticosteroids on blood flow velocity in gastric microvessels of muscular, submucosal and mucosal coats it was used intravital microfilming by means of a dark-field contact epiobjective. Stress (water immersion + restraint) induces an ulceration, a decrease in the systemic arterial blood pressure (3 h after stress onset) and a decrease in blood flow velocity in the gastric microvessels (3 h after stress onset). In rats with insufficient corticosteroid production stress-induced ulceration, a decrease in blood pressure and gastric blood velocity were more greater than in rats with intact PACS. Replacement corticosterone therapy corrected all parameters. The results revealed that antiulcerogenic effect of stress-induced glucocorticoid production is realised owing to normalisation of gastric blood supply which is provided by an increase in systemic blood pressure.