[Influence of anxiogenic stress upon severity of alloxan-induced pancreatic and hepatic damage].

4 episodes of immobilization stress caused anxious and depressive behavioral disorder in rats, accompanied by decreased sensitivity of pancreatic tissue to alloxan-induced damage, and simultaneously increased sensitivity of hepatic tissue to alloxanogenic inflammatory effect. The latter shifts were accompanied by a more pronounced hyperglycemia. The paper discusses a probable role of hepatitis in hyperglycemic response to alloxan challenge associated with stressogenic anxiety.

Activation of apoptosis as a mechanism of thymus involution during repeated immobilization.

Lymphopenia preceded involution of the thymus during daily immobilization for 1 h. Hypoplasia of the thymus was associated with induction of apoptosis.

[Effect of rarely repeated immobilization episodes on hypoxia-tolerance and anxiogenic stress severity].

4 episodes of immobilization stress (60 minutes, once 72 hours) led to diminution of hypoxia tolerance and anxiety-depressive disorders of behavior. The later shifts were associated with decrease of IL-4 concentration and simultaneous increase of IL-6 level in blood serum. The stress-induced behavioral shifts appeared to correlate with IL-4 concentration in blood of stress-sustained rats.

[Effects of triamcinolone acetonide on leukocyte distribution in blood system, mononuclear liver infiltration, and immune response under conditions of stress-induced hypoxia in rats].

The effect of triamcinolone acetonide (2 mg/kg) on the distribution of morphologically mature leukocytes in the blood system, the mononuclear liver infiltration, and the immune response was studied in rats under conditions of stress-induced hypoxia. Administered under these conditions, the drug produces a less pronounced effect on the content of circulating lymphocytes, the lymphoid cell number in the bone marrow, and the number of hepatocytes and monocytes/macrophages in the liver. However, the post-stressor immunodepressant effect of triamcinolone acetonide was increased and accompanied by the development of hepatic damage.

The effects of anxiogenic stress on glucocorticoid sensitivity, glucose tolerance, and alloxan resistance in rats.

Four sessions of immobilization stress induced anxiogenic behavioral disorders in rats, which were accompanied by decreases in glucocorticoid sensitivity, increases in MAO-B activity in brain tissue, increases in tolerance to glucose loading, and decreases in resistance to acute hypoxia. Alloxan diabetes was accompanied by a decrease in behavioral activity of rats in the open field test, with an increase in cerebral MAO-B activity. Preceding anxiogenic stress increased the extent of the alloxan-induced increase in cerebral MAO-B activity and the accompanying abnormalities in the rats' behavior, and also potentiated the hyperglycemic effect of alloxan.