Fetal Infusions of Plasma Cause an Increase in Umbilical Vascular Resistance in Sheep

• Published in: Placenta (Eastbourne) 2006-08, Vol.27 (8), p.876-881
• Main Authors: Faber, J.J., Anderson, D.F., Jonker, S.S., Davis, L.E., Giraud, G.D.
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Blood Pressure - physiology; Blood Proteins - analysis; Blood Transfusion, Intrauterine; Embryology: invertebrates and vertebrates. Teratology; Female; Fetal arterial pressure; Fetal placental flow; Fetal placental resistance; Fetus - physiology; Fundamental and applied biological sciences. Psychology; Infusions, Intra-Arterial; Placental Circulation - physiology; Plasma; Pregnancy; Renin - blood; Sheep, Domestic; Umbilical Arteries - physiology; Vascular Resistance - physiology
• ISSN: 0143-4004; 1532-3102
• DOI: 10.1016/j.placenta.2005.09.003

Earlier studies suggested that the fetal placental circulation is relatively inert with fetal placental flow increasing or decreasing with perfusion pressure. Subsequent studies have demonstrated that the placenta may not be an unreactive vascular bed. The present study was undertaken to determine if plasma infusion-induced hypertension increased fetal placental flow in proportion to the driving pressure across the fetal placental circulation. Six fetal sheep were operated on at 118–122 days to place intravascular catheters and a flow sensor on the common umbilical artery. Starting 6 days later, the fetuses were infused with adult sheep plasma. During the 7-day-long infusion period, they received a total of 1515 ± 217 (SD) ml of fluid and 93.2 ± 12.0 g of protein. Fetal plasma protein concentrations increased from 34.2 ± 2.3 to 77.0 ± 9.7 g/l ( P < 0.0001). Fetal arterial blood pressures rose from 42 ± 3 to 59 ± 4 mmHg ( P < 0.01) and venous pressures rose from 2.2 ± 0.5 to 4.8 ± 0.8 mmHg ( P < 0.01). In spite of the large increase in driving pressure, fetal placental blood flow remained (statistically) constant (627 ± 299 ml/min and 552 ± 221 ml/min) while fetal umbilical resistance increased from 0.077 ± 0.038 to 0.115 ± 0.053 mmHg min/ml ( P < 0.01). On day 7, plasma renin activity had fallen from 6.7 ± 4.2 ng/(ml/h) at preinfusion control to 0.6 ± 0.6 ng/(ml/h) ( P < 0.05) and plasma angiotensin-II concentration had fallen from 33.2 ± 26.6 to 6.2 ± 3.9 pg/ml, although this fall was not statistically significant ( P = 0.07). Fetal placental flow did not increase with increased driving pressure across the fetal placental circulation. The increase in fetal placental resistance may be a response to the increase in arterial pressure since there was no increase in flow.