Dual messenger function for prostaglandin E2 (PGE2) in human placenta.
There is periparturitional increase of prostaglandin E2 (PGE2) in the plasma and amniotic fluid of humans. PGE2 increases uterine contractions and also increases uterine blood flow to sustain the contractions. A question arises as to what role PGE2 plays in human placental circulation. It may regulate feto-placental blood flow and closure of placental resistance vessels at parturition. Therefore, we have investigated (a) the release of PGE2 into fetal and maternal circulations, and (b) the influence of PGE2 on the feto-placental pressure in the isolated perfused cotyledon of normal human term placenta. The placental cotyledon was perfused with aerated. (21% O2, 5% CO2) Krebs-Ringer bicarbonate buffer (pH 7.4, 37 degrees C) containing 2% albumin on both maternal (230 ml, 12 ml/min., 0.6" Hg) and fetal (93 ml, 1.75 ml/min., 1.75" Hg) sides in a closed recirculating system. In one group of cotyledons, perfusion samples (2 ml) were collected at regular intervals from both perfusates for 3 hrs. and PGE2 was determined in aliquots (0.5 ml) of samples by a specific radioimmunoassay. In a second set of cotyledons, exogenous PGE2 was administered into fetal perfusate, and pressure was monitored as a function of time. These experiments gave the following results: 1) During the initial 20 min., a constant level of PGE2 (2.3-4.4 pg/ml) was maintained in both perfusates. At 3 hrs., the concentrations increased to about 110 ng/ml on the fetal side and 30 ng/ml on the maternal side. The total amount of PGE2 accumulated in the fetal and maternal reservoirs reached to 10.16 and 7.03 ng, respectively. 2) PGE2 (10-150 ng/ml) increased the feto-placental perfusion pressure in a concentration dependent manner. At 150 ng/ml, the pressure increased to 125-240% of control pressure observed at the beginning of the experiment. These studies suggest that a) placental trophoblast has the capacity for the synthesis and release of PGE2 into fetal and maternal circulations; b) PGE2 exhibits differential effects in the placental and uterine blood vessels, vaso-constriction in placental vessels and vasodilation in uterine blood vessels, and (c) PGE2 exhibits dual effects on blood vessels possibly by activating two different subtypes of PG-receptors.
Sastry
B V
BV
Department of Anesthesiology, Vanderbilt University School of Medicine, Nashville, TN 37232-2125, USA.
Hemontolor
M E
ME
Chance
M B
MB
Johnson
R F
RF
D000328:Adult; D015237:Dinoprost / Q000378:metabolism; D015232:Dinoprostone / Q000378:metabolism / Q000502:physiology*; D005260:Female; D006801:Humans; D066298:In Vitro Techniques; D007743:Labor, Obstetric / Q000502:physiology; D008431:Maternal-Fetal Exchange / Q000235:genetics; D010477:Perfusion; D010920:Placenta / Q000098:blood supply / Q000502:physiology*; D011247:Pregnancy; D011312:Pressure; D011982:Receptors, Prostaglandin / Q000145:classification / Q000502:physiology; D014590:Uterine Contraction / Q000502:physiology; D014599:Uterus / Q000098:blood supply / Q000502:physiology; D014661:Vasoconstriction / Q000502:physiology; D014664:Vasodilation / Q000502:physiology
D011982:Receptors, Prostaglandin; D015237:Dinoprost; D015232:Dinoprostone