妊娠中期巨细胞病毒感染加重妇女胎盘子叶血流的解剖学特征

I. Gorikov
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引用次数: 0

摘要

的目标。目的:对妊娠中期巨细胞病毒感染(CMVI)加重的妇女胎盘子叶血流进行解剖学描述。材料和方法。研究人员对117个胎盘进行了研究,其中101个来自足月妊娠妇女,16个来自早产妇女。在所有病例中,CMVI导致慢性代偿性(CCPI)、亚代偿性(CSPI)和失代偿性胎盘功能不全(CDPI)的发展。共分为5组:第一组为巨细胞病毒(CMV)血清阴性足月妊娠妇女胎盘30块;第二组——27个胎盘来自慢性CMVI急性期患者,启动CCPI的发展;第3 - 23个胎盘来自CMVI加重导致CSPI形成的妇女;第4 - 21个胎盘来自CMVI加重患者,导致CDPI发展并延长妊娠至分娩期;第5 - 16个胎盘来自慢性CMVI急性期的妇女,启动CDPI的形成和流产。通过脐带静脉注射造影剂(在干油上涂红铅漆)来评估胎盘子叶的血流。使用RUM-20M“Sapphire”仪器获取x射线血图。结果。结果表明,子叶的总数在不同的研究群体中没有差异。在第一组中,血流对比良好的解剖形态为21.4±2.17,血管对比较弱的解剖形态为- 9.3±0.47,静脉、动脉和绒毛毛细血管无对比的解剖形态为- 2.9±0.22。在第二组胎盘中,与第一组相比,子叶的数量没有差异,子叶中血管清晰可见,未检测到。而血管对比差的解剖形态增加了1.51倍(p<0.05)。第三组胎盘与第二组相比,具有血管网络轮廓清晰的子叶比例减少了1.97倍(p<0.001),解剖形态增加了2.34倍,血流对比差(p<0.001)。第四组与第三组相比,血管清晰可见的子叶数量减少了2.05倍(p<0.001),解剖形态增加了1.44倍(p<0.01),其中x线静脉造影未确定血管。与第4组相比,第5组血液对比良好的子叶的出现频率低2.83倍(p < 0.01)。结论。随着CMVI在妊娠中期的加重,导致CDPI的形成,与胎盘中的CCPI和CSPI相比,由于CMV的直接促内皮和介导作用,子叶血流减少更常被检测到。这是胎盘缺血的解剖学基础,也是流产发生的病理机制之一。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Anatomical characteristics of the placental cotyledon bloodstream in women with exacerbation of cytomegalovirus infection during the second trimester of gestation
   Aim. To give an anatomical description of the placental cotyledon bloodstream in women who had an exacerbation of cytomegalovirus infection (CMVI) in the second trimester of gestation.   Materials and methods. A study was conducted on 117 placentas, of which 101 were from women with full-term pregnancy and 16 from women with premature birth. In all cases, CMVI led to the development of chronic compensated (CCPI), subcompensated (CSPI) and decompensated placental insufficiency (CDPI). 5 groups were identified: the first group consisted of 30 placentas from women with full-term pregnancy seronegative for cytomegalovirus (CMV); the second – 27 placentas from patients who had an acute phase of chronic CMVI, initiating the development of CCPI; the third – 23 placentas from women with exacerbation of CMVI, leading to the formation of CSPI; the fourth – 21 placentas from patients with an exacerbation of CMVI, which caused the development of CDPI and prolongation of pregnancy to the term of delivery; the fifth – 16 placentas from women with an acute phase of chronic CMVI, initiating the formation of CDPI and miscarriage. The assessment of the bloodstream of cotyledons of the placenta was carried out by injection of contrast (red lead-paint on dryingoil) through the vein of the umbilical cord. To obtain X-ray phlebograms, the apparatus RUM-20M “Sapphire” was used.   Results. It was shown that the total number of cotyledons did not differ in the studied groups. In the first group, anatomical forms with a well-contrasted bloodstream were 21.4±2.17, with weakly contrasted vessels – 9.3±0.47, and with no contrast in the veins, arteries and capillaries of the villi – 2.9±0.22. In the placentas of the second group, in comparison with the first one, no differences were found in the number of cotyledons, in which blood vessels were clearly visualized and not detected. However, the number of anatomical forms with poorly contrasted vessels increased by 1.51 times (p<0.05). The placentas of the third group in comparison with the second one were characterized by a decrease by 1.97 times (p < 0.001) in the proportion of cotyledons with a clear contouring of the vascular network and an increase in anatomical forms with a poorly contrasted bloodstream by 2.34 times (p<0.001). In the fourth group, in comparison with the third group, the number of cotyledons with clear visualization of vessels decreased by 2.05 times (p<0.001), and the number of anatomical forms increased by 1.44 times (p<0.01), in which X-ray phlebography did not determine the vasculature. In the fifth group compared to the fourth one, cotyledons with a well-contrasted bloodstream were found 2.83 times less frequently (p < 0.01).   Conclusion. With an exacerbation of CMVI in the second trimester of gestation, leading to the formation of CDPI, in comparison with CCPI and CSPI in the placenta, a reduction of blood flow in cotyledons is more often detected as a result of direct endotheliotropic and mediated effects of CMV. This is the anatomical basis of placental ischemia and one of the pathogenetic mechanisms for the development of miscarriage.
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