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Source: Longo LD. Respiratory gas exchange in the placenta. In: Fahri LE, Tenney SM, Eds., Handbook ofphysiology. Section 3: The respiratory system, Vol. IV, Gas exchange, pp. 351-401. Bethesda, MD: American Physiological Society, Washington, D.C., 1987. With permission.

Source: Longo LD. Respiratory gas exchange in the placenta. In: Fahri LE, Tenney SM, Eds., Handbook ofphysiology. Section 3: The respiratory system, Vol. IV, Gas exchange, pp. 351-401. Bethesda, MD: American Physiological Society, Washington, D.C., 1987. With permission.

state at a lower set-point. Progesterone also increases the sensitivity of the chemoreceptors for PO2, but this change is only evident in intense exercise or in hypoxic conditions such as high altitude. Thus, as already noted for cardiovascular and renal homeostasis, a signal arising in the ovaries and placenta readjusts the set-point for a normally operating negative feedback system.

Resetting the steady-state level of PCO2 in maternal blood benefits the developing fetus by facilitating the transfer of CO2 from the fetal to the maternal circulation. PCO2 equilibrates rapidly across the placental barrier by diffusion of CO2 in the form of the uncharged, dissolved gas. Its rate of diffusion depends the steepness of the concentration gradient between fetal blood in the umbilical artery and maternal blood in the intervillous space. By lowering the PCO2 in maternal blood, a steep concentration gradient is created while allowing fetal PCO2 and blood pH to be maintained at a level that is favorable for rapid cellular growth and development. The small increase in PO2 is of little consequence for oxygen delivery to the fetus, because maternal hemoglobin is already virtually saturated at the PO2 that prevails in nonpregnant women. However, the rapid rate of CO2 transfer across the placental barrier and the resulting transfer of hydrogen ion increase the rate of oxygen delivery to the fetus through operation of the Haldane and Bohr effects (see Chapter 20). The decrease in PCO2 in fetal capillary blood as it traverses the terminal villi increases the affinity of hemoglobin for oxygen, and hence its degree of saturation at the low partial pressure of oxygen of intervillous blood. At the same time, the increase in PCO2 in the intervillous space facilitates the unloading of oxygen from maternal hemoglobin. Simultaneously, the diffusion of CO2 across the placental barrier raises the pH of placental capillary blood and lowers that of intervillous blood to provide a similar effect on hemoglobin loading of maternal and fetal blood.

Gas exchange across the placenta is analogous to gas exchange in the lungs; the arterial supply to the placenta is low in O2 and high in CO2; after equilibration with maternal blood in the intervillous space, umbilical venous blood has taken on O2 and delivered CO2. Table 1 presents normal values of oxygen, carbon dioxide, and hydrogen ion concentrations in the maternal and fetal circulations in late pregnancy. Although PO2 and CO2 equilibrate quickly across the placental barrier, partial pressures of these gases in the umbilical veins differ radically from values in the uterine artery and even the uterine veins. Differences between uterine and umbilical venous blood can be accounted for in part by the relatively high rate of O2 extraction and CO2 production by the syncytiotrophoblast and by the relatively large areas of the placenta that are unavailable for exchange. It is important to note that despite the low PO2 and the metabolic activity of the syncytiotrophoblast, the oxygen content of umbilical venous blood is quite similar to that of maternal arterial blood. This is possible because of the higher content of hemoglobin in fetal than maternal blood and the greater affinity of fetal hemoglobin for oxygen. It is also noteworthy that PCO2, bicarbonate, and pH in umbilical venous blood are all in the same range as found in arterial blood of nonpregnant subjects (see Chapter 31).

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