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      • KCI등재후보

        Vasculosyncytial membrane in relation to syncytial knots complicates the placenta in preeclampsia

        K. Devi Sankar,P. Sharmila Bhanu,Sujatha Kiran,B. A. Ramakrishna,V. Shanthi 대한해부학회 2012 Anatomy & Cell Biology Vol.45 No.2

        The vasculosyncytial membrane (VSM), primary site of fetomaternal exchange is formed when syncytiotrophoblast surrounds the terminal villi and make a close contact with capillaries. Some syncytiotrophoblast forms thin single layer of villous and some syncytial nuclei become piled up to form the syncytial knots (SKs). Undoubtedly there is a clear-cut inverse relation between villous VSM and fetal hypoxia. In preeclampsia (PE) the hypoxia injury disrupts the syncytial architecture which in turn initiates other complications of PE. Present study was designed to observe the morphological and histomorphometric features of 84 placentas from control and PE (42 each) collected from Department of Obstetrics and Gynecology. Neonatal weight and placental weight were reduced in PE than the controls but the feto-placental index did not differ. The SK density and VSM thickness was found to be increased and was statistically significant in PE cases. In relation to SKs, the VSM thickness was twofold increased than the controls and was statistically significant. The SKs in the present study were classified as type-1, 2a, 2b, and 3. Type 1 was found to be 62% in control and 47% in PE, type 2a and 2b were 38% in control and 37% in PE, and type 3 was in 8% of PE cases. All the parameters of present study reveal the adverse effects of PE influencing on both morphological and microscopical features of the placenta resulting in fetal hypoxia.

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        Histomorphological and morphometrical changes of placental terminal villi of normotensive and preeclamptic mothers

        K. Devi Sankar,P. Sharmila Bhanu,K. Ramalingam,Sujatha Kiran,B. A. Ramakrishna 대한해부학회 2013 Anatomy & Cell Biology Vol.46 No.4

        Placental morphology and cellular arrangement are altered in maternal diseases such as preeclampsia (PE) in which oxygen delivery from the mother to the fetus is greatly disturbed, ultimately resulting in cellular oxidative stress. The present study was conducted at the Department of Anatomy and included 112 placentas (56 each from mothers with and without PE [controls]) collected at the Department of Obstetrics and Gynecology. A histological study was performed using hematoxylin and eosin staining. The morphology of stem and terminal villi (TV) was studied, and the surface area and diameter of TV and capillaries were measured. The gross placental morphometrical study revealed that the mean placental weight, thickness, diameter, and surface area were significantly lower in placentas with PE than in controls. The histomorphometrical findings of the villous surface area and diameter were lower in placentas with PE, whereas the TV density was higher in placentas with PE than in controls, and the differences were significant (P<0.0001). In these TV, the diameter and density of fetal blood vessels of placentas with PE were significantly lower than those of controls (P<0.05). In conclusion, the both morphological and histological changes in PE placentas are indicative of the pathogenesis of maternal and fetal morbidity and mortality in women with PE. The observed and comparative histomorphometrical changes indicate a decline in all aspects of the PE placenta, except the number of TV.

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