EXPERIMENTAL MODELING OF FETAL GROWTH RETARDATION
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Abstract (English):
The pathophysiological mechanisms of fetal growth retardation can be established experimentally. However, modeling methods have disadvantages related to labor intensity, low reproducibility of the process, and high rates of antenatal fetal death. The development of a modeling method with signs similar to the clinical picture in pregnant women is of urgent importance. The purpose of the study: to develop an experimental model of fetal growth retardation using didrogesterone and a pathogenetic substantiation of the mechanism of development. Material and methods. 20 female Wistar rats were used as laboratory animals, of which group 1 (n=10) were pre–pregnant rats and didrogesterone modeling; group 2 (n=10) were pre-pregnant rats. In the first 14 days of the experiment, the rats received a mixture containing 0.5 mg of didrogesterone in the morning and evening. The concentrations of progesterone and corticoste rone were determined. On day 21, euthanasia was performed, fetuses and afterbirth were collected, and weight and histological structure were determined. The research analysis was carried out using the Statistica 10.0 program. Results. In group 1 rats, compared with group 2 rats, there was an increase in progesterone levels and a decrease in corticosterone concentration. A negative correlation was established between progesterone and corticosterone levels (r=0.862; p <0.05). The rats had lower fetal weight and length, and lower weight of the afterbirth. Placental macrophages were absent in the placentas. The mechanism of fetal development delay in the experimental model is related to the potential hepatotoxicity of didrogesterone. A decrease in corticosterone is associated with impaired glucocorticoid me tabolism in the liver. Didrogesterone can bind to glucocorticoid receptors. A low level of corticosterone before childbirth indicates a disorder of adaptive mechanisms. Low levels of corticosterone lead to placental disorders. Conclusion. The method of modeling fetal delay is confirmed by the results of growth, fetal weight, and histological examination of the placenta. The mechanism of occurrence is related to the hepatotoxicity of progestogens

Keywords:
fetal growth retardation, modeling, dydrogesterone
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