Relations of catecholamine and prostaglandin contents in the blood of rats exposed to acute stress and during adaptation to stress

• Published in: Biulleten' eksperimental'noi biologii i meditsiny Vol. 109; no. 6; p. 534
• Main Authors: Pshennikova, M G, Kuznetsova, B A, Shimkovich, M V, Saprygin, D B, Meerson, F Z
• Format: Journal Article
• Language: Russian
• Published: Russia (Federation) 01-06-1990
• Subjects: Acute Disease; Adaptation, Physiological; Animals; Catecholamines - blood; Dinoprost - blood; Dopamine - blood; Epinephrine - blood; Epoprostenol - blood; Immobilization; Male; Norepinephrine - blood; Prostaglandins - blood; Prostaglandins E - blood; Rats; Rats, Inbred Strains; Stress, Physiological - blood; Stress, Physiological - physiopathology; Thromboxane A2 - blood
• ISSN: 0365-9615

In Wistar male rats, 1-h acute immobilization stress resulted in the increased plasma adrenalin, noradrenaline and dopamine in approximately 13, 8 and 23 times, respectively. Plasma PGF2 alpha increased in 3.5 times while PGE remained unchanged; this resulted in the decreased PGE/PGF2 alpha relation in 2.8 times. The PGI2/TXA2 relation also decreased in 1.5 times due to a more pronounced growth of TXA2 than that of PGI2. In rats adapted to the repeated stress (12 sessions), the plasma catecholamine level was higher than that in control but 2-3 fold lower than in unadapted rats after acute single stress. In this situation, PGE was increased by 70% as compared to the control. This is why PGE/PGF2 alpha relation was similar to the control whereas the level of PGF2 alpha increased. PGI2 increased by 53% and TXA2--in two times as compared to the control. In these rats, acute stress induced neither plasma catecholamine enhancement nor PGE/PGF2 alpha relation decrease in comparison with the initial levels; the TXA2 content was increased but it was by 33% less than that in unadapted rats exposed to such stress. One can suggest that the decreased activation of adrenergic system respondent to acute stress in unadapted rats is associated with the increase in plasma PGE and PGI2 which are known to limit the catecholamine release from adrenergic terminals and their harmful effects.