[The role of the mediator and hormonal links of the sympathetic-adrenal system in the anxiolytic effect of close to physiological doses of L-thyroxine under stress].

Abstract

Objective: To study an effect of small doses of L-thyroxine on the level of anxiety in animals under stress and to analyze the role of the mediator and hormonal links of the sympathetic-adrenal system in its implementation.

Material and methods: The study was performed on 78 white outbread male rats. Stress was modeled using the «time deficit» method. Chemical sympathectomy was performed by intraperitoneal injection of guanetidine at a dose of 30 mg/kg for 28 days. Bilateral adrenalectomy was performed according to the method of Y.M. Kabak. L-thyroxine was injected intragastrically for 28 days in small doses (1.5-3 µg/kg). The level of anxiety was determined in the «open field» test. The content of iodine-containing thyroid hormones (ICTH) in the blood serum was evaluated by the enzyme immunoassay.

Results: It has been found that stress activates thyroid function (an increase in the concentration of ICTH by 23-44%, p<0.01) and increases the level of anxiety in animals (an increase in the total resting time by 21%, p<0.05 and the resting time in periphery - by 25%, p<0.01). Chemical sympathectomy does not affect the growth of anxiety in rats who have undergone stress, whereas adrenalectomy contributes to its increase (an increase in the total resting time and the resting time in periphery by 15 and 14%, p<0.05). The injection of L-thyroxine minimizes the increase in the content of ICTH in the blood (by 16-27%, p<0.05) and has an anxiolytic effect under stress (prevents an increase in the total resting time and the resting time in periphery). Both chemical sympathectomy and, especially, adrenalectomy somewhat minimize, but do not completely prevent the implementation of the anti-anxiety effect of L-thyroxine under stress.

Conclusion: In the formation of the anti-anxiety effect of ICTH, their central stress-limiting influence is important, limiting the mobilization of both the mediator and hormonal links of the sympathetic-adrenal system. The role of the latter in the implementation of the stress-protective effect of thyroid cancer is not decisive.