STATE CALCIUM-PHOSPHORUS METABOLISM AND BONE TISSUE IN EXPERIMENTAL HYPOTHYROIDISM

In experimental hypothyroidism caused by intragastric administration merkazolila daily dose of 2,5 mg/100 g body weight for 21 days in male albino adult rats determination of serum levels of thyroid hormone, thyrotropin, total calcium, phosphorus, magnesium, bone alkaline phosphatase, C-terminal telopeptide of collagen type I. The thighs animal control and experimental groups studied histological structure diaphysis H&E stain. The development of hypothyroidism is confirmed by a decrease in the content of thyroxine and triiodothyronine, with increased secretion of thyroid-stimulating hormone. With the development of merkazolil hypothyroidism in serum levels of bone resorption marker C-terminal telopeptides of type I collagen is reduced slightly, while the bone formation marker – izoferment alkaline bone phosphatase activity decreases significantly. These results reflect the disturbances of bone remodeling with a slowing phase of formation of new bone. Thus, the level C-terminal telopeptide bone collagen in intact animals was 0,87±0,06 ng/ml, test group of rats decreased to 0,78±0,04 ng/ml (p>0,1), the activity of bone alkaline phosphatase at merkazolil hypothyroidism decreased to 4,8±0,36 U/l, in intact rats was equal to 6,1±0,46 U/l (p<0,05). This leads to violations of the histological structure of bone tissue. The diaphysis of tubular bones of rats with hypothyroidism in the study of the microstructure revealed areas of thinning of cortical bone mass loss of tissue deformation and demineralization osteones, luminal narrowing osteones and other features characteristic of dysplastic developing osteoporosis.