The dynamic placenta: II. Hypothetical model of a fetus driven transplacental water balance mechanism producing low apparent permeability in a highly permeable placenta.
In vitro and isotopic studies in vivo have reported the paradox that the human placenta is highly permeable, water exchanging at 3.6 litres per hour at 35 weeks of gestation, but clinical measurements in vivo show net transfer is minimal, around 2 ml/day. Current theories are based on osmotic pressure balances, but changes in maternofetal hydrostatic pressure change much faster than osmotic factors could respond. An alternative explanation might be that net transfer is not in fact the result of passive mechanisms, but is actively controlled by the fetus itself. The fetus is well equipped to monitor changes in blood volume, such as via sensors in venous and atrial stretch receptors to control ANF and hence urine production. Transplacental water regulation requires modification of transvillus pressures. Placental sub-chorial arteries and veins (of extra-embryonic origin) have different sensitivities from fetal body tissues to some vasoactive substances, and stem villous veins have unusually well developed vascular smooth muscle. It is thus theoretically possible for the fetus to modify subchorial venous resistances, and hence villous capillary pressure with a suitable circulating placental venous constrictive agent. A computer modelling study was undertaken using a fictitious placental venous constricting agent "fictensin", considered to be released by the fetus in proportion to disturbance of vascular volume. The effective placental permeability fell in proportion to the tightness of this fetal control mechanism, suggesting that the apparent placental permeability measured in vivo is a measure of fetal control, not true permeability. However, the range of compensatory pressures that the fetus can produce by this means is limited and failure of such a mechanism could allow flooding or dehydration of the feto-placental unit. This may shed new light on disorders such as polyhydramnios and fetal hydrops.
Sebire
N J
NJ
Department of Histopathology, Camelia Botnar Laboratories, Great Ormond Street Hospital, Great Ormond Street, London WC1N 3JH, UK. SebirN@gosh.nhs.uk
Talbert
D
D
D000818:Animals; D001810:Blood Volume; D002196:Capillaries; D005260:Female; D005333:Fetus / Q000502:physiology*; D006801:Humans; D008431:Maternal-Fetal Exchange; D008954:Models, Biological; D010539:Permeability; D010920:Placenta / Q000378:metabolism / Q000502:physiology*; D021041:Placental Circulation; D011247:Pregnancy; D014469:Umbilical Arteries; D014471:Umbilical Veins; D014655:Vascular Resistance; D014661:Vasoconstriction; D014882:Water-Electrolyte Balance