Concepto de RCIU, Clasificación: PEG, RCIU. Etiología, Fisiopatología, Diagnóstico, Manejo, Pronóstico. Concept of IUGR, Classification: SGA. Dra. Sofía Córdoba V. Residente II Año Ginecología y Obstetricia HCG Tutor: Dr. Manrique Leal M. Fisiopatología del RCIU mediante el. 14 ago. Objetivos específicos: • Compreender a fisiopatologia da doença, sua RCIU: Gemelares monocoriônicos > Dicoriônicos > gestações únicas.
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Study of the evolution of the placenta and fetal pancreas in the pathophysiology of growth retardation intrauterine due to restricted maternal diet Discipline of Obstetrics, Faculdade de Medicina de Botucatu, UNESP, Botucatu, Brazil.
Intrauterine growth retard IUGR continues to be a significant perinatology problem at the end of this century. The nature of the etiologic agent, the time when the attack eciu during pregnancy and its duration affect the type of IUGR.
To study the evolution of fetal pancreas and placenta between the 18th and 21st day of pregnancy in rats submitted to maternal protein-calorie restriction. Randomized controlled trial on laboratory animal. Forty-one normoglycemic pregnant Wistar rats.
Rats were divided into six experimental groups according to their access to food and date of fisoipatologia section 18th or 21st day: Maternal protein-calorie malnutrition caused intrauterine growth retard IUGR after the 18th day of pregnancy.
Dietary restriction after the 3rd day of pregnancy led to low placental glycogen concentrations on the 18th day and disappearance on the 21st day. Fisiopatoloogia pathophysiology of IUGR due to maternal protein-calorie restriction in rats is related to lower placental rcij and low placental glycogen stores.
Experimental research carried out in Botucatu Brazil has demonstrated that fetuses with IUGR are obtained using models fisilpatologia protein-calorie malnutrition, of maternal arterial hypertension and of severe maternal diabetes. An interesting aspect has been observed in the model of diabetes and pregnancy in rats: A more in-depth study of the placenta and pancreas of newborn rats has permitted the understanding of the deviations in fetal growth occurring in the presence of moderate and severe diabetes.
Newborn rats with severe diabetes showed increased glycogen deposition in the placenta from the 18th to the 21st day of pregnancy. Calderon 12 demonstrated that the endocrine pancreas of newborn rats with moderate diabetes has large islets with increased insulin production, as observed by immunohistochemistry using specific antibodies.
In the pancreas of newborn rats with severe diabetes the islets are large but have no insulin-positive cells and therefore their insulin production is depleted. Since moderate diabetes is a model of fetal macrosomia, we may infer that maternal hyperglycemia causes fetal hyperglycemia and hyperinsulinism.
This leads to the removal of glycogen fisiopatoloogia in the placenta which, converted into energy, increases the weight of newborn rats. In severe diabetes, a IUGR model, severe maternal hyperglycemia causes intense fetal hyperglycemia leading to depletion of fetal pancreatic function.
The lack of insulin production by the fetal pancreas at the end of pregnancy does not permit the removal of glycogen stores from the placenta and the fetus does not grow in an adequate manner. The use of a restricted fusiopatologia for the treatment rdiu diabetic rats 13 showed that non-diabetic pregnant control rats had IUGR, a fact previously observed by others. Study of the evolution of the fetal pancreas and of the placentas of normal pregnant rats submitted to a restricted diet, which has proved to be a model for Fiisopatologia, 17 would permit the evaluation of this physiopathology.
The general objective of the fisioopatologia investigation was to study the physiopathology of intrauterine growth retardation in fetuses in pregnant rats submitted to protein-calorie malnutrition, on the basis of evolution of the placenta and of the fetal pancreas.
After pregnancy was confirmed, rcik the rats were assigned at random to the following experimental groups according to the diet used and the gestational age at the time of resolutioni. Calculation of food fiisopatologia. After removal of the uterus and separation of the placenta, newborn rats were weighed and classified as small SGAappropriate AGA and large LGA for gestational age of 18 and 21 days as compared to the mean and Standard for the control group.
The placentas were separated from their membranes, weighed and processed for histopathological study morphology and histochemistry. The material was embedded in paraffin, sectioned and stained with hematoxylin-eosin HE. Histochemical fisiopatologka was performed by the periodic acid Schiff PAS reaction for the identification of glycogen deposits on the placental membrane on 18th and 21st days of pregnancy. The fetal pancreases were resected, pooled for each litter and processed for morphohistology.
The material was stained with HE and morphology was compared between the experimental groups. Ten Langerhans islets per slide were analyzed in terms of size, borders and quantity of vacuoles in the cell cytoplasm. Photomicrographs of the major histopathologic and histochemical features of the placentas and of the fetal pancreases were obtained.
Data concerning newborn weight and placental weight were analyzed by fully randomized factorial analysis of variance. The 41 rats produced young; the mean number of newborns per rat was On the 18th day of pregnancy, mean newborn weight was higher in the group submitted to dietary restriction after the 3rd day.
When pregnancy was resolved on the 21st day, fetal weight was decreased in the group of pregnant rats submitted to dietary restriction, and more intensely in the group in which restriction was started after the 3rd day Figure 1.
The placentas of rats submitted to dietary restriction were larger than those of the control on the 18th day of pregnancy. At the end of pregnancy, the weight of the placentas of rats submitted to dietary restriction from the 1st day of pregnancy was the same as the weight of control rats and higher than that of the group submitted to dietary restriction after the 3rd day Figure 2.
Figure 1 – Mean weight of newborn rats from the control group, the group submitted to dietary restriction from the 1st day and the group submitted to dietary restriction after the 3rd day of pregnancy, as determined on the 18th and 21st days of pregnancy.
Figure 2 – Mean weight of the placentas from the control groups, the group submitted to dietary restriction from the 1st day and the group submitted to dietary restriction after the 3rd day of pregnancy, as determined on the 18th and 21st days of pregnancy. On the 18th day of pregnancy, no increase incidence of SGA newborn rats was observed in the restricted groups, compared to the controls.
When the restricted groups were compared with each other, the percentage of SGA young was higher in the group submitted to dietary restriction from the 1st day of pregnancy. On the 21st day there was a clear occurrence of retarded intrauterine growth in the young from malnourished mothers Figure 3.
Figure 3 – Percentage of small for gestational age newborn rats from the control group, the group submitted to dietary restriction from the 1st day and the group submitted to dietary restriction after the 3rd day of pregnancy, as determined on the 18th and 21st days of pregnancy.
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The pancreases of the newborn rats showed characteristics of pancreatic islet maturation that were similar for all six groups studied Table 1 and Figures 4 and 5.
Figure 5 – Pancreas of newborn rats obtained on the 21st day of pregnancy from the group receiving the diet ad libitum Athe group submitted to protein-calorie restriction from the 1st day B and the group submitted to protein-calorie restriction from the 3rd day of pregnancy C – in Hematoxylin-Eosin. The thickness of the placental exchange surface decreased fjsiopatologia the 18th to the 21st day of pregnancy in all groups studied, but the placentas did not differ in terms of quantity of cytotrophoblastic cells.
Placental glycogen stores were normal on the 18th day and decreased by the 21st day of pregnancy in the control groups and in the groups with dietary restriction introduced on the 1st day of pregnancy. In contrast, placental glycogen fidiopatologia had already decreased by the 18th day of pregnancy in rats submitted to dietary restriction on the 3rd day of pregnancy Table 2 and Figures 6 and 7.
Figure 6 – Placentas of rats receiving the diet ad libitum A and of rats submitted to protein-calorie restriction from the 1st day B and after the 3rd day of pregnancy Cobtained on the 18th rciuu of pregnancy – in Hematoxylin-Eosin and Periodic Acid Schiff. Fisiopatologiaa 7 – Placentas of rats receiving the diet ad libitum A and of rats submitted to fisiopatologiz restriction from the 1st visiopatologia B and after the 3rd day of pregnancy Cobtained on the 21st day of pregnancy – in Hematoxylin-Eosin and Periodic Acid Schiff.
Maternal protein-calorie restriction reduces offspring size. This is probably due to the vicarious action of the placenta occurring with its increased weight Figures 1 and 2.
The evolution of pregnancy up to the 21st day shows that fisiopatolofia restriction is a model for IUGR Figure 3 associated with decreased placental weight Figure 2confirming previous reports. The correlation of fetal weight with placental weight has been clinically documented in studies evaluating appropriate, small and large for gestational age newborns. Experimental studies on malnourished rats throughout pregnancy have demonstrated lower birth weight, a higher neonatal mortality rate, and placental damage consisting of reduced weight, number of cells and protein amounts.
In the present study, between the 18th and the 21st day of pregnancy the placenta showed a decrease in membrane thickness in all groups Table 2 and Figures 6 and 7.
Placental glycogen stores also decreased after the 18th day in the control groups and in the groups submitted to dietary restriction from the 1st day of pregnancy. In the groups submitted to dietary restriction after the 3rd day of pregnancy, glycogen stores were already smaller on the 18th day and disappeared by the 21st day of pregnancy Table 2 and Figures 6 and 7.
Histopathologic examination of the fetal pancreases did not shown the effects of maternal malnutrition Table 1 and Figures 4 and 5.
The present results show that the physiopathological mechanism of IUGR in the presence of maternal dietary restriction seems to differ from that occurring in diabetes. In diabetes, placental glycogen stores are not utilized and converted to energy for fetal growth, due to the lack of fetal insulin. The action of severe maternal hyperglycemia depletes the fetal pancreas, which loses the ability to produce insulin at the end of pregnancy.
Small placentas with low glycogen deposits seem to play the most important role in the etiology of IUGR due to protein-calorie malnutrition introduced after the 3rd day of pregnancy.
In the groups submitted to dietary restriction from the 1st day of pregnancy, fetal development was normal up to the 18th day because of the vicarious action of the placenta fisiopaatologia of the glycogen stores.
The fisiopafologia of maternal malnutrition up to the 21st day was associated with decreased fetal weight and increased incidence of intrauterine growth retardation even though placental weight was maintained and glycogen stores evolved normally. The present results permit us to explain the occurrence of IUGR due to protein-calorie malnutrition introduced after the 3rd day of pregnancy.
Maternal protein-calorie malnutrition was the cause of IUGR in rats, with the following physiopathologic peculiarities:. From the 18th to the 21st day, fetal weight reduced, with an increased incidence of SGA newborns without decreased stores of placental glycogen.
Protein-calorie restriction after the 3rd day of pregnancy reduced glycogen stores in the placenta and fetal development. Arch Latinoamer Nutr b;33 1: J Ped ;46 2: Faculdade de Medicina, Universidade Estadual Paulista. Diabetes and experimental pregnancy in rats: Course of maternal blood glucose levels and its repercussions on the blood glucose levels and pancreas of newborn pups.
Brazilian J Med Biol Res ; Arch Latinoamer Nutr a;33 1: Protein caloric deficiency in rats. Br J Nutr ; J Ped ;46 1: Not declared Last received: Risiopatologia the contents of this journal, except where otherwise noted, is licensed under a Creative Commons Attribution License.
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