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

Abstract

Our aim was to study the mechanisms of hypoxia development at pregnancy associated with cytomegalovirus infection (CMVI). 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. 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. 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.