Vascular adaptive mechanisms to hypoxic conditions in the human placenta defined by maternal hematological parameters

摘要

Vasculogenesis and angiogenesis during implantation and placentation are crucial for successful gestation. Sufficient capillary network formation provides optimal development of the embryo and fetus. Abnormalities in microvessels growth pattern can lead to such pathological conditions as: intrauterine growth retardation (IUGR), PE/EC (preeclampsia/eclampsia), anemia or GDM (gestational diabetes mellitus). Vascular endothelial growth factor (VEGF) and placenta growth factor (P1GF) are main cytokines regulating vasculogenesis and angiogenesis in the human placenta mostly through flt-1 and flk-1 receptors. Oxygen tension also stimulates fetoplacental vascularity development, therefore hypoxia stimulates villi hypercapillarisation. Maternal anemia (best characterized by a reduction in hemoglobin concentration) during pregnancy can also influence the pattern of vascular growth. However there is only limited knowledge about placental morphological adaptation changes to a decrease in the oxygen carrying capacity of the blood. In the present study we investigated whether selected maternal blood parameters such as hemoglobin (Hb) concentration, hematocrit (Ht) values and erythrocyte count (RBC) influence density of placental microvessels (flt-1, flk-1 receptors expression, vascular/extravascular tissular index-V/EVTI) and its correlation with the birth weight. Inverse correlation of flt-1, flk-1 expression and V/EVTI with maternal Hb concentration, Ht values and erythrocyte count was observed in each trimester of pregnancy. Mean V/EVTI correlates positively with flt-1 expression and the birth weight. Possibly, P1GF mainly affects placental vascular development under hypoxic conditions (as it binds only to flt-1).