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Fetal growth retardation (FGR) is a major cause of child morbidity and mortality, and is also an important medical and social problem due to a wide range of pregnancy complications and negative outcomes in the postnatal period. The results of recent studies indicate that chronic arterial hypertension causes a number of pathological changes in a pregnant woman’s organism, in particular, it increases the risk of FGR.The wide knowledge about the pathogenesis of placental dysfunction and FGR allow to establish that the development of these pathologies is primarily caused by the changes in uterine and placental blood circulation, which leads to metabolic disorders. The important etiological reasons for FGR also include social and biological factors, the influence of narcotic substances, insufficient nutrition, alcohol abuse, tobacco smoking, as well as the use of coumarin or derivatives. The mother’s older age is also a risk factor for the FGR development.Over the past decades, both clinical and experimental studies have established that FGR, caused by the influence of the unfavorable environment of the uterus, is a risk factor for the development of hypertension, as well as various diseases in adults. There are a lot of evidences that support the association of FGR with an increased risk of hypertension in adults, but the mechanisms underlying these processes remain unclear. Both clinical and basic scientific studies have confirmed the theory of intrauterine programming of arterial hypertension in adults. That is why many countries have developed programs for the prevention of FGR. Scientific researches indicate a close relationship between social adaptation and the birth of children with low body weight.The absence of indices decrease in perinatal morbidity and mortality by FGR shows the difficulties caused by polyetiological factors and certain pathogenetic mechanisms of the mentioned complication. Today, the search for an effective pathogenetically based therapy of this pathology continues, which indicates the need for further researches, and the development and implementation of approaches to the prevention of FGR will improve the perinatal putcomes.
Fetal growth retardation (FGR) is a major cause of child morbidity and mortality, and is also an important medical and social problem due to a wide range of pregnancy complications and negative outcomes in the postnatal period. The results of recent studies indicate that chronic arterial hypertension causes a number of pathological changes in a pregnant woman’s organism, in particular, it increases the risk of FGR.The wide knowledge about the pathogenesis of placental dysfunction and FGR allow to establish that the development of these pathologies is primarily caused by the changes in uterine and placental blood circulation, which leads to metabolic disorders. The important etiological reasons for FGR also include social and biological factors, the influence of narcotic substances, insufficient nutrition, alcohol abuse, tobacco smoking, as well as the use of coumarin or derivatives. The mother’s older age is also a risk factor for the FGR development.Over the past decades, both clinical and experimental studies have established that FGR, caused by the influence of the unfavorable environment of the uterus, is a risk factor for the development of hypertension, as well as various diseases in adults. There are a lot of evidences that support the association of FGR with an increased risk of hypertension in adults, but the mechanisms underlying these processes remain unclear. Both clinical and basic scientific studies have confirmed the theory of intrauterine programming of arterial hypertension in adults. That is why many countries have developed programs for the prevention of FGR. Scientific researches indicate a close relationship between social adaptation and the birth of children with low body weight.The absence of indices decrease in perinatal morbidity and mortality by FGR shows the difficulties caused by polyetiological factors and certain pathogenetic mechanisms of the mentioned complication. Today, the search for an effective pathogenetically based therapy of this pathology continues, which indicates the need for further researches, and the development and implementation of approaches to the prevention of FGR will improve the perinatal putcomes.
The objective: to study pathological changes and compensatory-adaptive reactions in the structural and ultrastructural components of the placental barrier in pregnant women with gestational arterial hypertension, who received magnesium preparations. Materials and methods. 100 patients with gestational hypertension were examined. The presence of magnesium deficiency in these women was determined by the results of our questionnaires.Pathomorphological and electronic microscopic examination of 32 placentas of patients with gestational hypertension was carried out. 12 placentas of them were from pregnant women who received the proposed management of pregnancy, which included magnesium drugs (I group), and 11 placentas – from patients with risk of preeclampsia, who were observed with the use of standard approaches of pregnancy for women with the risk of preeclampsia (II group). Control group included the results of pathomorphological and electronic microscopic study of 9 placentas from healthy women.Results. Placental of women with gestational hypertension have structural features, which is manifested by the mosaic change of placental barrier in the form of uneven circulatory disorders with hemorrhages and stasis (at the ultrastructural level) in the fetal microvessels of the villi, reducing the placental functional area (rapprochement of the villi), presence of stromal sclerosis villi, foci of pathological immaturity, increase in calcium salts (mineral dystrophy) on the background of compensatory reactions. Electronic microscopic study of the placentas in the I group revealed an increase in the compensatory-adaptive reactions of the placenta – thinning of the placental barrier, activation of cytotrophoblast cells in the placental barrier, increase the number of syncytiocapillary membranes in terminal villi with syncytiotrophoblast organic activation, increase in the number of ribosomes, the appearance of orthodox configuration of mitochondria, increasing the number of capillary membranes and thinning of syncytia, reducing the number of sludge phenomena in microvessels, which leads to an increase in the possibility of nutrient transfer from mother to fetus, etc.Conclusions. The use of the proposed therapy, which involves magnesium, diosmin and others substances, leads to a significant decrease in the frequency of detection of pathological changes in structural and ultrastructural components of the placental barrier and increased compensatory-adaptive reactions which can be considered the result of the positive impact of the proposed therapy on the placental ultrastructural elements in women with risk of preeclampsia.
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