A single transcranial electrostimulation of rats results, as does acute stress, in a fourfold elevation of plasma corticosterone, whereas after a course of several electrostimulations plasma corticosterone is not elevated and a threefold rise in plasma [~-endorphin is recorded. Rats that undergoing a course of transcmmal electrostimulations and then subjected to an immobilization stress do not show any rise in plasma corticosterone.

Control and acutely stressed August rats have corticosterone levels 62% and 15% higher, respectively, than their Wistar counterparts, indicating that the activity of stress-mediating hypothalamic-pituitary-adrenal system in August rats is higher. On the other hand, the intensity of stress reactions and, consequently, the degree of activation of this system in August rats are 40-50% lower, as is the blood level of creatine phosphokinase. During adaptation to stress, August and Wistar rats show a similar decrease in the stress reaction and in its damaging effects. However, judging from the blood corticosterone/insulin ratio, adaptation to stress in August rats coincides with intensification of catabolic processes and a reduction in the efficiency of energy production.

No abstract

Adaptation to physical load protects against stress and other damage. It is suggested that this protection is associated with activation of prostaglandins E (PGE) and 12 (PGI2). Plasma contents of PGE2, PGI2, and thromboxane A 2 (TxA2) and the severity of stress reaction are measured in male Wistar rats adapted to swimming. Training increases the concentrations of these prostaglandins and the prostaglandin/TxA 2 ratio, reduces almost 2-fold the severity of stress reaction as assessed by the plasma corticosterone concentration and corticosterone/insulin ratio. After stress, the PGI 2 and PGIJTxA_, in adapted rats were, respectively, 33 and 31% higher than in unadapted. These findings suggest that prostaglandins are involved in the reduction of stress reaction.