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Placental dysfunction as a key element in the pathogenesis of preeclampsia

Henning Schneider
Henning Schneider
   | Jan 02, 2018
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Article Category: Special contribution
Published Online: Jan 02, 2018
Page range: 309 - 316
Received: Aug 30, 2017
Accepted: Sep 06, 2017
DOI: https://doi.org/10.34763/devperiodmed.20172104.309316
Keywords
© 2017 Henning Schneider, published by Sciendo
This work is licensed under the Creative Commons Attribution 4.0 International License.

Fig. 1

This picture is from the Carnegie Collection and shows normal development of a human pregnancy at Day 9 post conception. Implantation is almost complete and the conceptus is at the blastocyst stage showing two cell lineages, the embryoblast and the trophoblast. By fusion of uninucleate cytotrophoblast the multinucleate syncytiotrophoblast (Syn) is formed. Lacunae (L) inside the syncytiotrophoblast are forerunners of the intervillous space, which at this stage has no open connection with the uteroplacental vasculature. At the right lower corner the syncytiotrophoblast has eroded the wall of an endometrial gland (Gl), which releases its secretions into the lacuna. Adapted from [6].
This picture is from the Carnegie Collection and shows normal development of a human pregnancy at Day 9 post conception. Implantation is almost complete and the conceptus is at the blastocyst stage showing two cell lineages, the embryoblast and the trophoblast. By fusion of uninucleate cytotrophoblast the multinucleate syncytiotrophoblast (Syn) is formed. Lacunae (L) inside the syncytiotrophoblast are forerunners of the intervillous space, which at this stage has no open connection with the uteroplacental vasculature. At the right lower corner the syncytiotrophoblast has eroded the wall of an endometrial gland (Gl), which releases its secretions into the lacuna. Adapted from [6].

Fig. 2

Conversion of the spiral arteries. On the left: a spiral artery in the first trimester, endovascular trophoblast is shown in green and extravascular or interstitial trophoblast in blue. On the right: a spiral artery in the second trimester with complete transformation. Both, endovascular trophoblast acting from the lumen of the vessel and the interstitial trophoblast acting from the outside are involved in the process of transformation. Adapted from [9].
Conversion of the spiral arteries. On the left: a spiral artery in the first trimester, endovascular trophoblast is shown in green and extravascular or interstitial trophoblast in blue. On the right: a spiral artery in the second trimester with complete transformation. Both, endovascular trophoblast acting from the lumen of the vessel and the interstitial trophoblast acting from the outside are involved in the process of transformation. Adapted from [9].

Fig. 3

Start of maternal blood flow in hysteroscopy video recordings. The picture on the left is taken before 10 weeks when the intervillous space contains clear fluid but no blood. The picture on the right is taken at the end of the first trimester, after the spiral arteries have been opened and maternal blood has entered the intervillous space. Adapted from [11].
Start of maternal blood flow in hysteroscopy video recordings. The picture on the left is taken before 10 weeks when the intervillous space contains clear fluid but no blood. The picture on the right is taken at the end of the first trimester, after the spiral arteries have been opened and maternal blood has entered the intervillous space. Adapted from [11].

Fig. 4

Three-dimensional reconstruction based on serial sections of a specimen from a hysterectomy performed after delivery at term. Myometrial (M) and endometrial (E) segments of the spiral artery are shown. Before opening into the intervillous space the terminal coil of the vessel is funnel-shaped and has a diameter of 2-3 mm. Adapted from [12].
Three-dimensional reconstruction based on serial sections of a specimen from a hysterectomy performed after delivery at term. Myometrial (M) and endometrial (E) segments of the spiral artery are shown. Before opening into the intervillous space the terminal coil of the vessel is funnel-shaped and has a diameter of 2-3 mm. Adapted from [12].

Fig. 5

Based on this reconstruction Graham Burton and colleagues speculated on rheological consequences of the conversion of the spiral arteries. On the left, conditions in normal pregnancy are shown. The funnel-shaped terminal dilation of the spiral artery serves to slow down the speed of uteroplacental blood flow to 10 cm/s as it enters the intervillous space. From the central cavity of the lobule the maternal blood evenly disperses through the villous tree. An estimated transit time of 25-30 s is sufficient to allow diffusion of an adequate amount of oxygen from erythrocytes to the trophoblast. On the right, conditions found in abnormal pregnancies are shown. With incomplete conversion of the spiral arteries, maternal blood enters the intervillous space at a much higher speed of 1 to 2 m/s, anchoring villi are torn off the basal plate and echogenic cysts form underneath the chorionic plate. The oxygen exchange is impaired by the reduced transit time. Shedding of microparticles from the surface of the villous trophoblast into the intervillous space is also increased. Adapted from [12].
Based on this reconstruction Graham Burton and colleagues speculated on rheological consequences of the conversion of the spiral arteries. On the left, conditions in normal pregnancy are shown. The funnel-shaped terminal dilation of the spiral artery serves to slow down the speed of uteroplacental blood flow to 10 cm/s as it enters the intervillous space. From the central cavity of the lobule the maternal blood evenly disperses through the villous tree. An estimated transit time of 25-30 s is sufficient to allow diffusion of an adequate amount of oxygen from erythrocytes to the trophoblast. On the right, conditions found in abnormal pregnancies are shown. With incomplete conversion of the spiral arteries, maternal blood enters the intervillous space at a much higher speed of 1 to 2 m/s, anchoring villi are torn off the basal plate and echogenic cysts form underneath the chorionic plate. The oxygen exchange is impaired by the reduced transit time. Shedding of microparticles from the surface of the villous trophoblast into the intervillous space is also increased. Adapted from [12].

Fig. 6

In normal pregnancy, early placental development is characterized by the proliferation of villi, a process which is driven by angiogenesis. The trophoblastic enzymes hem oxygenase 1 (Hmox1) and cystathionine γ-lyase (Cth) generate gaseous signalling molecules carbon monoxide (CO) and hydrogen sulphide (H2S), which together with placental growth factor (PlGF), another product of trophoblast, provide a strong proangiogenic effect, also known as “Vascular Protection”. Ahmed and Ramma have proposed that in early onset preeclampsia intrinsic alterations in the biology of the trophoblast lead to an impairment of “Vascular Protection”. Due to an increased secretion of fms like tyrosine kinase 1 as soluble VEGF receptor (sFlt-1) as well as soluble endoglin together with a reduced production of PlGF “Vascular Protection” of normal pregnancy is replaced by “Vascular Dysfunction” of preeclampsia. Adapted from [13].
In normal pregnancy, early placental development is characterized by the proliferation of villi, a process which is driven by angiogenesis. The trophoblastic enzymes hem oxygenase 1 (Hmox1) and cystathionine γ-lyase (Cth) generate gaseous signalling molecules carbon monoxide (CO) and hydrogen sulphide (H2S), which together with placental growth factor (PlGF), another product of trophoblast, provide a strong proangiogenic effect, also known as “Vascular Protection”. Ahmed and Ramma have proposed that in early onset preeclampsia intrinsic alterations in the biology of the trophoblast lead to an impairment of “Vascular Protection”. Due to an increased secretion of fms like tyrosine kinase 1 as soluble VEGF receptor (sFlt-1) as well as soluble endoglin together with a reduced production of PlGF “Vascular Protection” of normal pregnancy is replaced by “Vascular Dysfunction” of preeclampsia. Adapted from [13].
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