Changes in the cerebral cortex and thyroid in the simulation of cerebral hypoperfusion and its combination with physical exercise

Cerebral hypoperfusion, as the main mechanism of age-associated diseases, is widespread, which leads to decreased work capacity in the most qualified segment of employees. The study aimed to analyze compensatory and adaptive reactions of the cerebral cortex, thyroid gland, and blood in cerebral hypoperfusion and its combination with short-term physical activity. Chronic cerebral hypoperfusion was modeled by permanent bilateral occlusion of the common carotid arteries. The study included 280 rats, of which 112 were subjected to daily short-term swimming as a model of rehabilitation measures. On days 1, 6, 8, 14, 21, 28, 35, 60, and 90 after surgery, the animals were subjected to the Morris water maze and open field tests. Histological sections of the brain and thyroid gland were examined. The concentrations of the active products of thiobarbituric acid, nitrites, and L-arginine in blood plasma were measured. The results showed that changes in the cerebral cortex and thyroid gland in the cerebral hypoperfusion model were characterized by a general stage: days 1–8, hypothyroid condition and death of cortical cells, cerebral hemispheres, predominantly neurons; weeks 2–3, stabilization, transition to the euthyroid condition, accompanied with thyrocyte desquamation, folliculogenesis, perifollicular hemocapillaries fullness, decreased functional activity of neurons, and astrocyte activation; weeks 4–5, incomplete adaptation, which is characterized by neurons approaching the vessels of the hemocirculatory channel and satellites sinking into the cytoplasm of neurons. Mosaicism of thyroid blood filling was also observed. After 3 months, degenerative changes in the cells of the cerebral cortex of the cerebral hemispheres appear, including a decrease in the numerical density of neurons and immunoreactive cells of glial fibrillar acid protein and a hyperthyroid state with signs of decompensation: plasmorrhagia and desquamation of the thyroid epithelium. Daily 15-min exercise with cerebral hypoperfusion demonstrated a neuroprotective effect, slowed down the progression of hypoxic and neurodegenerative changes, and reduced the concentration of nitrites and malondialdehyde in the blood and the levels of neuronal nitric oxide synthase in immunoreactive neurons.