[Mechanisms of hypoxia development during pregnancy and the disorder of fetus blood supply at cytomegalovirus infection].

M T Lutsenko, I A Andrievskaya, N A Ishutina, A G Mironenko
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引用次数: 17

Abstract

OBJECTIVE Our aim was to study the mechanisms of hypoxia development at pregnancy associated with cytomegalovirus infection (CMVI). METHODS 30 parturient women with CMVI relapse at the 25-28 weeks of pregnancy and their newborns were examined. Cytochrome C, Hsp-70, p53, Bcl-2 and caspase-3 in placenta homogenate were found out with serologic methods, the morphology of erythrocytes with cytophotometry, erythrocytes membrane proteins with disc-electrophoresis method, TBA-active products with V.B. Gavrilov's method, superoxide dismutase activity with spectrophotometry, 2.3-diphosphoglyceric acid (2.3 DPG) with I.S. Luganov's method, erythrocytes membrane microviscosity with fluorimethric method, oxyhemoglobin and methemoglobin with Evelyn and Malloy' method, and erythrocytes deformability with M. T. Lutsenko's method. RESULTS In blood erythrocytes of CMV-seropositive parturient women there was the decrease of cytoskeleton proteins: α- and β-spectrine was 1.14 times less, ankyrin was 1.62 times less, band 4. 1 protein was 1.29 times less; there was 1.87 times increase of antigen-binding glycophorin, 1.37 times growth of TBA-active products and 1.35 times drop of superoxide dismutase activity; the deformability index was 9.5 times less, 2.3 DPG was 1.22 times less and oxyhemoglobin was 1.06 times less. In placenta homogenate Bcl-2 was 1.5 times less, Hsp-70 was 2.5 times more, p53 was 6.1 times more, cytochrome C was 1.76 times more, caspase-3 was 3.86 times more. In umbilical cord blood erythrocytes 2.3 DPG was 1.3 times more and oxyhemoglobin was 1.06 times less. CONCLUSION The obtained data proves that CMVI relapse at 25-28 weeks of pregnancy causes the disorder of morphofunctional state of mother's blood erythrocytes and their ability to oxygenation, the development offetoplacental barrier, the decrease offetus oxygen blood supply and the development of intrauterine hypoxia.
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巨细胞病毒感染时妊娠期缺氧发育及胎儿血供紊乱的机制
目的:研究巨细胞病毒感染(CMVI)引起妊娠期缺氧的机制。方法:对30例妊娠25 ~ 28周CMVI复发的产妇及其新生儿进行检查。采用血清学方法检测胎盘匀浆中的细胞色素C、Hsp-70、p53、Bcl-2和caspase-3,采用细胞光度法检测红细胞形态,采用碟状电泳法检测红细胞膜蛋白,采用V.B. Gavrilov法检测tba活性产物,采用分光光度法检测超氧化物歧化酶活性,采用I.S. Luganov法检测2.3-二磷酸甘油酸,采用荧光法检测红细胞膜微粘度,采用荧光法检测胎盘匀浆中的细胞色素C、Hsp-70、p53、Bcl-2和caspase-3。用Evelyn和Malloy的方法测定氧合血红蛋白和高铁血红蛋白,用m.t. Lutsenko的方法测定红细胞变形能力。结果:cmv血清阳性孕妇红细胞中细胞骨架蛋白减少,α-、β-谱蛋白减少1.14倍,锚蛋白减少1.62倍,带4。1个蛋白少1.29倍;抗原结合糖蛋白增加1.87倍,tba活性产物增加1.37倍,超氧化物歧化酶活性下降1.35倍;变形性指数降低9.5倍,2.3 DPG降低1.22倍,氧合血红蛋白降低1.06倍。胎盘匀浆中Bcl-2含量低1.5倍,Hsp-70含量低2.5倍,p53含量低6.1倍,细胞色素C含量低1.76倍,caspase-3含量低3.86倍。脐带血红细胞DPG增高1.3倍,氧合血红蛋白增高1.06倍。结论:所获资料证实CMVI在妊娠25-28周复发导致母体红细胞形态功能状态及氧合能力紊乱,胎盘屏障发育,胎儿供氧血供减少,发生宫内缺氧。
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CiteScore
1.50
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0.00%
发文量
31
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