[The effects of desensitization of capsaicin-sensitive neurons on the blood flow in microvessels of the rat gastric serous muscular membrane with normal and insufficient contents of glucocorticoids].

The effects of desensitization of capsaicin-sensitive neurons on the blood flow velocity in microvessels of the gastric muscular membrane were investigated before and after indomethacin (35 mg/kg) administration in adrenalectomized rats with or without corticosterone replacement (4 mg/kg sc) and in sham-operated animals. Desensitization of capsaicin-sensitive neurons was performed with neurotoxic dose of capsaicin (20 + 30 + 50 mg/kg sc) two weeks before the experiment. Adrenalectomy was created one week before the experiment. The in vivo microscopy technique for direct visualization of gastric microcirculation and analysis of red blood cell (RBC) velocity was employed. Indomethacin decreased the RBC velocity. Adrenalectomy by itself profoundly decreased the RBC velocity, whereas corticosterone replacement prevented this effect. Desensitization of capsaicin-sensitive neurons did not influence the RBC velocity in sham-adrenalectomized rats; however, it induced further fall of both basal and indomethacin-induced RBC velocity in adrenalectomized rats that was prevented by corticosterone. We conclude that glucocorticoid hormones have a beneficial effect on the blood flow velocity in microvessels of the gastric muscular membrane in rats with desensitization of capsaicin-sensitive neurons.

[The adaptation-protective effect of corticosteroids on the rat gastric mucosa and its mechanism]. / Adaptatsionnyi zashchitnyi éffekt kortikosteroidov na slizistuiu obolochku zheludka krys i ego mekhanizm.

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.