Влияние малых доз L-тироксина на устойчивость к стрессу животных с экспериметально вызванным дефицитом симпатических нервных влияний

Abstract

Slight increase in catecholamine levels has an adaptive effect at stress. The role of the thyroid axis in adaptation to stress is also proved. However, it remains unclear whether the protective effect of iodine-containing thyroid hormones (ITH) in stress is mediated by catecholamines or this is direct action of ITH. The purpose of this research is to investigate the expression of the antistress effect of low doses of L-thyroxine at animals with a of sympathetic nervous influences caused in the experiment. The experiment was performed on 270 white unbread male rats weighing 220-240 g. Stress was modeled using the deficit method. L-thyroxine was injected in small, close to physiological doses (intragastriclly from 1.5 to 3 μg/kg for 28 days). Guanetidine was injected intraperitoneally (30 mg/kg for 28 days). The intensity of the stress response was studied by changes in: 1) the relative mass of the adrenal glands, thymus and spleen; 2) the level of corticosterone and insulin in the blood, the value of the corticosterone-insulin coefficient; 3) the state of the gastric mucosa. Motor activity of rats was evaluated in the open field test. Physical endurance of animals was studied by the time they were on a rotating roller. The results obtained were processed using nonparametric methods with the help of the program Statistica 10.0 (Stat Softinc., STA999K347156-W). Chemical desimpatization prevents the stimulation of thyroid function under stress and, at the same time, determines a greater decrease in the body's stability under these conditions. The combined administration of L-thyroxine and guanetidine has a protective effect under stress at rats with an intact nervous system. However, compared to them, this effect is less expressed, which indicates that catecholamines play a role in its realization, but ITH have a critical significance. The protective effect of small doses of L-thyroxine under stress is partially mediated by catecholamines, but to a greater extent by ITH itself.