The placenta in the integrated physiology of fetal volume control

Abstract

Almost all water that enters the conceptus of the sheep enters via the placenta. The forces that drive water are hydrostatic and osmotic. The placental channels that allow water to cross into the fetus have not been identified by microanatomic means. Although an "equivalent pore" system can account for the diffusional entry of small hydrophilic solutes, it can be calculated that the filtration coefficient of this system is too small to account for the demonstrated trans-placental water flows. It is possible that a second much less numerous system of large pores permits the flow of water, but that is by no means certain. The placenta does not control the amount of water that enters the conceptus; nor does any other single fetal structure. And water entry is not dependent on the volume of water already present. However, the combined physiological properties of the fetal heart, kidneys, somatic tissues and placenta constitute a consistent explanation of fetal water volume control.

Fig. 1. Dependency of fluid exchange between maternal and fetal placental circulations on the concentration of angiotensin-II in fetal plasma

The values for fluid exchange on the abscissa are not exactly known, except for the value of zero.

Fig. 2. Relation between fetal renal artery pressure and fetal plasma renin activity

From Binder & Anderson, (1992). Note logarithmic ordinate.

Fig. 3. Relation between fetal arterial blood pressure and fetal plasma angiotensin-II concentrations

Numerical values are based on data from Giraud et al., 2005).

Fig. 4. Experimentally determined relation between filling pressure and stroke volume in the fetal heart

From Thornburg & Morton, (1986).

Fig. 5. Relation between fetal venous pressure and biventricular cardiac output, expressed per kg fetal weight

At constant arterial oxygen content, an increase in cardiac output causes a disproportionate increase in arterial pressure (solid line). This signifies a resistance to flow that is much lower at low flows than at high flows (the sloped dashed lines are lines of constant resistance, low resistance at the left end of the curve and high resistance at the right end). Autoregulation translates minor changes in flow into large changes in pressure.

Fig. 6. Autoregulation of flow

At constant arterial oxygen content, an increase in cardiac output causes a disproportionate increase in arterial pressure (solid line). This signifies a resistance to flow that is much lower at low flows than at high flows (the sloped dashed lines are lines of constant resistance, low resistance at the left end of the curve and high resistance at the right end). Autoregulation translates minor changes in flow into large changes in pressure.

Fig. 7. Juxtaposition of Figs. 1,3,5,6

The figure shows that the mechanisms are interdependent.

Fig. 8. Relation between arterial pressure and plasma renin activity

From Binder & Anderson, (1992). Filled symbols from 3 fetuses; open symbols from the same 3 fetuses as lambs in the 1^st week after delivery.