ALTERATIONS IN PLACENTA REDOX-STATUS DURING EXPERIMENTAL MODEL OF HYPOXIA-INDUCED PREECLAMPSIA.

An important pathogenetic link of preeclampsia (PE) is hypoxia of uterine-placental tissues, accompanied by damage of the vascular endothelium and the release of vasoactive mediators, violate vascular tone and microcirculation in the maternal organism and placenta and development of a number of pathological processes in the mother's and fetus body. The aim of the study was to establish metabolic abnormalities of oxidative metabolism of the placenta during experimental model of PE (uterine/placental hypoxia). Studies were performed in pregnant Wistar rats. Chronic reductions in uterus placental perfusion in rats, reduced uterine perfusion pressure by 35% to 45% during first trimester (10-th day) gestation was reached by placing a silk ligature around the abdominal aorta below the renal arteries and narrowed aortic lumen, in the third of its diameter (0.2 mm). All rats undergoing surgical procedures were anesthetized with 2% ether. The animals were sacrificed under ether anesthesia on 25th day of pregnancy under the Ether anesthesia and extirpation of genital system with a fetus was made. The histopathological study of placenta tissue, investigation of free NO, it's metabolites (HbNO and FeSNO) and lipoperoxides content and blood antioxidant enzymes (catalase and superoxide dismutase) activity was performed. The study's results indicate that during experimental model of PE oxidative stress conditions in rats developed, free nitric oxide content significant decreased and increased content of nitric oxide complexes with hemic and non-hemic iron (FeSNO, HbNO). These data indicate that nitrosilation is crucial mechanism by which NO regulates placental metabolic pathways. By histopathological studies revealed an infringement of the process placentation, involution, destructive changes in varying degrees in the placenta of rats of hypoxia group in the end of the third trimester. These data indicate, that disorders of the placental blood supply are responsible for the alteration of its oxidative metabolism, development of the placenta's hypoxia, intensification of oxidative stress and disturbance of placenta's blood vessels proliferation and blood circulation, that brings the father dangerous complications of fetus.