Lucenko M T, Andrievskaya I A, Dolzhikova I V
Vestn Ross Akad Med Nauk. 2016;71(3):177-82.
Determine the characteristics of placental energy metabolism and to establish its role in the development of placental insufficiency at an exacerbation of cytomegalovirus (CMV) infection in 25–28 weeks of gestation.
In a prospective study of the case-control type included pregnant, delivery on term of 37–38 weeks. The sample of 50 pregnant women, including 25 CMV-seropositive with exacerbation of CMV infection at 25–28 weeks of gestation and with the titer of IgG antibodies to CMV 1: 1600 at the time of the study and 25 CMV-seronegative women the same pregnancy. The study was conducted at the obstetric department of pathology of pregnancy and laboratory «Etiopathogenesis mechanisms and recovery processes with non-specific lung diseases» Far Eastern Scientific Center of Physiology and Pathology of Respiration together with the urban maternity ward at City Hospital in the period from 2014 to 2015. The activity of pyruvate dehydrogenase, α-ketoglutarate dehydrogenase and a dehydrogenase lipoic acid was determined by histochemical methods on cryostat sections of fresh frozen tissue placenta by the method of R. Lilly. Evaluation of the intensity of histochemical reactions carried out by the program cytophotometry Scion. The morphology of the placenta was studied in paraffin sections stained with hematoxylin Böhmer-eosin, van Gieson’s picrofuchsin and alcian blue by Steedman.
Exacerbation of CMV infection at 25–28 weeks of gestation leads to a decrease in the intensity of the histochemical reaction of pyruvate dehydrogenase in 2.4 times, lipoic acid dehydrogenase — in 2.9 times, and α-ketoglutarate dehydrogenase — in 1.5 times in the syncytiotrophoblast villous placenta. The placental morphological structure study showed villi in a state of death or necrotic changes, as well as increasing the number of avascular immature villi. In the maternal part of the placenta were marked constriction clearances, hypertrophy of muscle and connective tissue layers blood vessels.
The findings suggest that the exacerbation of CMV infection at 25–28 weeks of pregnancy causes a decrease in the intensity of energy metabolism in the placenta by suppressing the activity of the enzymes α-ketoglutarate dehydrogenase and pyruvate dehydrogenase complex, which is accompanied by disturbances of the morphological structure of the placental barrier, the development of placental insufficiency.
确定胎盘能量代谢特征，并确定其在妊娠25 - 28周巨细胞病毒（CMV）感染加重时胎盘功能不全发展中的作用。
在一项病例对照型前瞻性研究中，纳入了足月妊娠37 - 38周分娩的孕妇。样本包括50名孕妇，其中25名CMV血清学阳性，在妊娠25 - 28周时CMV感染加重，研究时CMV IgG抗体滴度为1:1600，以及25名相同孕周的CMV血清学阴性孕妇。该研究于2014年至2015年期间，在远东呼吸生理学与病理学科学中心妊娠病理产科和实验室“非特异性肺部疾病的发病机制及恢复过程”以及市立医院的城市产科病房进行。采用R. Lilly法，通过对新鲜冷冻组织胎盘的低温切片进行组织化学方法，测定丙酮酸脱氢酶、α - 酮戊二酸脱氢酶和硫辛酸脱氢酶的活性。利用Scion细胞光度测量程序对组织化学反应强度进行评估。采用Steedman法，对用苏木精 - 博默伊红、范吉森苦味品红和阿尔辛蓝染色的石蜡切片进行胎盘形态学研究。
妊娠25 - 28周时CMV感染加重导致合体滋养层绒毛胎盘的丙酮酸脱氢酶组织化学反应强度降低2.4倍，硫辛酸脱氢酶降低2.9倍，α - 酮戊二酸脱氢酶降低1.5倍。胎盘形态结构研究显示绒毛处于死亡或坏死状态，无血管未成熟绒毛数量增加。在胎盘母体部分可见明显的狭窄间隙、血管肌肉和结缔组织层肥大。
研究结果表明，妊娠25 - 28周时CMV感染加重通过抑制α - 酮戊二酸脱氢酶和丙酮酸脱氢酶复合体的活性，导致胎盘能量代谢强度降低，同时伴有胎盘屏障形态结构紊乱，进而发展为胎盘功能不全。
