Arterial maternal

Placental transfer of trichloroethylene occurs in animals. Trichloroethylene inhaled by pregnant sheep and goats, at levels used to induce analgesia and anesthesia, is rapidly distributed into the fetal circulation, with peak levels occurring approximately 40-50 minutes after maternal exposure (Helliwell and Hutton 1950). The concentration of trichloroethylene in umbilical vein blood was comparable to that found in the maternal carotid artery. 

Animal data include an inhalation study in rabbits that resulted in an increased incidence of retroesophageal right subclavian artery in the fetuses (Hayes et al. 1985), and an oral study in rats that resulted in an increased incidence of an extra rib (NTP 1987). The data were considered sufficient to derive an acute-duration inhalation MRL of 0.8 ppm, based on a NOAEL of 300 ppm for lack of developmental effects in rabbits. It would be useful to have additional information on the developmental effects of 1,4-dichlorobenzene by inhalation and oral exposure in relation to maternal toxicity. There are currently no data available for the dermal route. Information on the developmental effects of dermal exposures would be useful if dermal absorption and systemic distribution of 1,4-dichlorobenzene could be demonstrated in toxicokinetic studies. 

Ruhle W, Graf Von Ballestrem CL, Pult HM, Gnirs J (1995) [Correlation of cotinine levels in amniotic fluid, umbilical arterial blood and maternal blood.] Geburtshilfe Frauenheilkd, 55 156-159 (in German). 

Two umbilical arteries from the foetus carry blood to the placenta and a single umbilical vein returns blood from the placenta back to the foetus. The functions of the placenta in pregnancy are to supply oxygen and nutrients from the maternal circulation to the foetus and to remove waste materials, such as urea and carbon dioxide, from foetal blood. 

Pregnancy is also associated with a partially compensated respiratory alkalosis that may affect the protein binding of some drugs. Respiratory changes in pregnancy include a decrease in arterial partial pressure of carbon dioxide to 30.9 mm Hg, most likely due to the effect of progesterone (23,24). In compensation, serum bicarbonate decreases, and maternal serum pH increases slightly to 7.44 (23). 

The placenta develops from a portion of the zygote and thus has the same genetic endowment as the developing fetus (78). The embryonic/fetal component consists of trophoblastic-derived chorionic villi/ which invade the maternal endometrium and are exposed directly to maternal blood in lake-like structures called lacunae. These villi create the large surface area necessary for maternal-fetal transfer in what becomes the intervillous space of the placenta. Here the maternal blood pressure supplies pulsatile blood flow in jetlike streams from the spiral arteries of the endometriunX/ to bathe the chorionic villi and allow for transfer of gaseS/ nutrientS/ and metabolic products. Biologically/ the human placenta is classified as a hemochorial placenta because maternal blood is in direct contact with the fetal chorionic membrane. It is this membrane that determines what is transferred to the fetus. 

Tuberculous hepatic infections are transmitted pre-/perinatally via the mnbihcal vein or the amniotic fluid maternal placenta tuberculosa is a precondition for both infections. The hepatic artery and the portal vein as well as the hepatopetal lymph vessels serve as postnatal infection routes. 

The hemodynamic effects of ritodrine have been assessed in 12 fetuses by cardiac and extracardiac Doppler sonography (1). Ritodrine significantly increased maternal and fetal heart rates, left cardiac stroke volume, and cardiac output. There was also an increase in the pulsatility index of the middle cerebral artery and a fall in the pulsatility index of the umbilical artery during ritodrine infusion. The authors suggested that ritodrine vasodilates fetal vessels in the placenta. 

For sensitized mothers with an at-risk fetus, serial titers are performed on maternal serum every month until 24 weeks gestation, then every 2 weeks thereafter. If a critical titer anti-D is detected, then ultrasound Doppler measurements are used to determine the peak velocity of blood flow in the fetal middle cerebral artery. Higher velocity is a strong indicator of fetal anemia. In addition, amniocentesis is performed to assess the bilirubin concentration in amniotic fluid. 

Comparison of Steroid Concentrations (/ig/100 ml) in Plasma from the Maternal Peripheral Vein (PV), Umbilical Cord Artery (CA),... 

From Table 5 it will be seen that the cortisol cortisone ratio of 0.7 1 in mixed arterial and venous umbilical cord blood is a complete reversal of the ratio of 11 1 in maternal blood. This change could be produced by the placenta because blood milked from a cord at delivery is predominantly venous. James (J3) has measured the two steroids in samples of pooled venous and pooled arterial plasma although he found the same levels (7, ag/100 ml) in each for cortisol, the level of cortisone was lower in the artery (10.5 jug/lOO ml) than in the vein (14.0 jug/lOO ml), indicating a supply of cortisone from the placenta. The considerable activity of... 

It will be seen from Table 3 that lower levels of estrone and estradiol, but higher levels of estriol, are found in cord blood compared with maternal blood. Estrone and estradiol can be formed from DHA-sulfate reaching the placenta from the fetus (B25) or the mother (B4, B25, S18, W2). These steroids are then secreted by the placenta into the maternal and fetal compartments. Estrone and estradiol reaching the fetus by the umbilical vein can be 16a-hydroxylated to form estriol, but most of the estriol is probably formed by placental aromatization of the large amounts of 16a-OH-DHA sulfate synthesized by the fetus (D6). Estriol is rapidly catabolized by infants (see Section 4.1.3), but if this is so for the fetus, the similar concentration in arterial and venous cord blood is difficult to explain, though a small amount of the estriol in the arterial blood may have been formed by the fetus from estrone and estradiol supplied by the placenta. 

Simmer, H. H., Easterling, W. E., Jr., Pion, R. J., and Dignam, W. J., Identification of dehydroepiandrosterone sulfate in fetal blood and quantification of this hormone in cord arterial, cord venous and maternal peripheral blood in normal pregnancies at term. Steroids 4, 125-135 (1964). 

Following intravenous injection in the mother, placental transfer of Metubine iodide occurs rapidly, and, after 6 minutes, the fetal plasma concentration is approximately one-tenth the maternal level. Metocurine does not inhibit vagal transmission or sympathetic ganglionic blockade, and therefore produces minimal hemodynamic changes in humans. The relatively stable heart rate and blood pressure associated with its use make it a useful agent for patients with coronary artery disease and hypertension. 

In the placenta a volume of oxygen sufficient for fetal needs must diffuse across the membranes from maternal to fetal blood during the short time the two circulations are in close contact. This oxygen transfer is a function of several factors which include uterine and umbilical arterial 02 partial pressures, maternal and fetal placental blood flow rates, the 02 capacity and 02 affinity of maternal and fetal hemoglobin, the diffusing capacity of the placenta, the amount of C02 exchanged, and the vascular arrangement of maternal to fetal vessels. 

Normal values for the various determinants of 02 transfer are necessary for quantitative analysis of the exchange process. Some values— e.g., those for the maternal and fetal arterial 02 tensions, 02 capacities, and 02 affinities—are fairly well defined. Others—e.g., the diffusing capacity and maternal and fetal placental blood flows—are less well determined. 

When these modifications are incorporated (14), the integration time on the computer increases severalfold (from 0.15 to 0.95 sec per integration step), but the results obtained for a maternal arterial p02 of 95 mm Hg differed from those of Figure 5 by less than 3%. The simpler form of the equations ignoring physically dissolved 02 was therefore... 

Effect of Varying Fetal Arterial 02 Tension. Placental exchange has usually been considered limited by either maternal and fetal blood flows or by diffusion. The present analysis suggests umbilical arterial p02 (Pf) is a third and very important factor, based on the observation... 

Figure 9. The effects of changes in maternal arterial 02 tension on maternal and fetal end-capillary pq2 and mean rate of Oz exchange. Moderate increases in maternal arterial p0 above normal values (95 mm Hg) increase end-capillary Poo and mean 02 exchange rate only slightly, hut decreases in maternal arterial p02 produce substantial decrease in 02 exchange and end-capillary values.

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