Oxygenation of the placenta and its role in pre-eclampsia.

Abstract

Proper oxygenation of the placenta and hence the embryo/fetus is essential for a successful pregnancy. During the first trimester of pregnancy the partial pressure of oxygen in the placenta and the embryo is very low and does not exceed 20mmHg. At the end of the first trimester maternal blood flow towards the placenta is established leading to a sudden increase in placental oxygenation to about 50-60mmHg. This level of oxygenation is keptuntil delivery. One of the numerous hypotheses to describe the etiology of preeclampsia, which is still the most cited hypothesis today, is based on a failure of extravillous trophoblast to invade the uterine spiral arteries in the placental bed. This in turn is believed to result in placental hypoxia and subsequently to damage of the villous trophoblast. Following this hypothesis, there is a series of events following these hypoxic conditions of the placenta. There is a large number of articles published that have investigated the effect of different oxygen concentrations on the phenotype of trophoblasts in vitro and have used this data to corroborate the hypothesis above. Unfortunately, one important aspect has not been addressed until recently: What is the placental oxygen concentration in placental pathologies such as preeclampsia in vivo? All studies that have tried to elucidate the placental oxygen concentration have done this indirectly, since direct measurements of placental oxygen in the third trimester of pregnancy have been defined as unethical. Not a single of such studies has revealed that oxygenation of the placenta in pregnancy pathologies is decreased. At the same time a number of studies have shown that in intra-uterine growth restriction (IUGR) placental oxygenation is increased rather than decreased. This has been shown to be true in the presence and absence of preeclampsia. This data clearly disprove the above hypothesis and should open our minds to decipherthe realcauses of preeclampsia.