Intravascular infusions of plasma into fetal sheep cause arterial and venous hypertension

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Abstract
Fetal volume control is driven by an equilibrium between fetal and maternal hydrostatic and oncotic pressures in the placenta. Renal contributions to blood volume regulation are minor because the fetal kidneys cannot excrete fluid from the fetal compartment. We hypothesized that an increase in fetal plasma protein would lead to an increase in plasma oncotic pressure, resulting in an increase in fetal arterial and venous pressures and decreased angiotensin levels. Plasma or lactated Ringer solution was infused into each of five twin fetuses. After 7 days, fetal protein concentration was 71.2 ± 4.2 g/l in the plasma-infused fetuses compared with 35.7 ± 6.3 g/l in the lactated Ringer-solution-infused fetuses. Arterial pressure was 68.0 ± 3.6 compared with 43.4 ± 1.9 mmHg in the lactated Ringer solution-infused fetuses ( P < 0.0003), whereas venous pressure was 4.8 ± 0.3 mmHg in the plasma-infused fetuses compared with 3.3 ± 0.4 mmHg in the lactated Ringer solution-infused fetuses ( P < 0.036). Six fetuses were studied on days 0, 7, and 14 of plasma protein infusion. Fetal protein concentration increased from 31.1 ± 1.5 to 84.8 ± 3.8 g/l after 14 days ( P < 0.01), and arterial pressure increased from 43.1 ± 1.8 to 69.1 ± 4.1 mmHg ( P < 0.01). Venous pressure increased from 3.0 ± 0.4 to 6.2 ± 1.3 mmHg ( P < 0.05). Fetal heart rate did not change. Angiotensin II concentration decreased, from 24.6 ± 5.6 to 2.9 ± 1.3 pg/l, after 14 days ( P < 0.01). Fetal plasma infusions resulted in fetal arterial and venous hypertensions that could not be corrected by reductions in angiotensin II levels.

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