Neonatal Placental barrier

Neonatal Cocaine freely crosses the placental barrier, and prenatal exposure to cocaine alters neurobehavioral development in rat pups (Sobrian et al. 1990). The effects on humans exposed prenatally to cocaine is a complicated matter, because so many other concurrent factors contribute to development. Common confounds are prenatal care and maternal polydrug use. Prenatal cocaine use is associated with reduced gestational age, birth weight, body length, and head circumference (Richardson et al. 1999). In children exposed prenatally to cocaine, some studies have shown behavioral differences evident at 1 to 3 years of age (Richardson et al. 1993 Richardson 1998). Associations are also made with impulsivity and attention deficits at age 6 (Leech et al. 1999). 

Labor - Narcotics cross the placental barrier and can produce depression of respiration and psycho-physiologic effects in the neonate. 

All sedative-hypnotics cross the placental barrier during pregnancy. If sedative-hypnotics are given during the predelivery period, they may contribute to the depression of neonatal vital functions. Sedative-hypnotics are also detectable in breast milk and may exert depressant effects in the nursing infant. 

Opioid analgesics are often used during obstetric labor. Because opioids cross the placental barrier and reach the fetus, care must be taken to minimize neonatal depression. If this occurs, immediate injection of the antagonist naloxone will reverse the depression. The phenylpiperidine drugs (eg,... 

As ketorolac crosses the placental barrier, it should not be used in pregnant women. When it is given to mothers during labor, it significantly inhibits platelet aggregation in the neonate (SEDA-14, 94). 

GI distress (NVD), phototoxicity, and hemolysis in GPDH deficiency. Avoid in third trimester because they cross placental barrier and may displace bilirubin from plasma proteins in neonates —> kernicterus. 

CNS drugs readily cross the placental barrier and enter the fetal circulation. Concerns during pregnancy include possible effects on fetal development and the potential for drug effects on the neonate if CNS drugs are used near the time of delivery. 

The protection afforded the fetus by the mother occurs by transfer of immunoglobulins from the maternal circulation to the fetal circulation across the placental barrier (the chorioallantoic placenta). This is not true of all species of mammals. In some the yolk sac appears to be the major route across which immunoglobulins are transferred (e.g., rabbit, guinea pig, and mouse). In others, such as goats, cows, and sheep, no immunoglobulins are transferred during intrauterine life but are obtained by the neonate from maternal colostrum by absorption across the gut. In some mammals (mouse, rat, dog) both pre- and postnatal transfer occurs (Schlamowitz, 1976). 

Molybdenum can cross the placental barrier. High levels of molybdenum in the diet of the mother can increase the molybdenum concentration in the liver of the neonate [26]. The level of molybdenum in milk is also influenced by the level of dietary molybdenum [9]. 

Distribution of mercury in fetal and neonatal tissues has been extensively investigated in guinea pigs exposed to mercury vapor in utero (Yoshida et al. 1987, 1990). Though mercury vapor easily crosses the placental barrier, mercury concentration in the fetal or neonatal brain is lower than that in the maternal brain after in utero exposure. On the contrary, much higher concentrations of mercury were found in the fetal liver than in the maternal liver. Most of the mercury in the fetal liver was found in the fraction of MT in the cytosol. The hepatic concentration of MT is known to increase drastically in the late gestational and early neonatal period. It seems likely that mercury vapor which entered the fetus is readily oxidized in the fetal liver, then trapped by the abundant MT, thus resulting in a lower distribution of mercury to the other fetal tissues. 

A carefully monitored single case (51 ) has documented the relationship of maternal to foetal lithium levels in a woman treated with lithium for the second and third trimester of pregnancy. The close similarities in maternal, umbilical and neonatal lithium levels confirm the absence of a placental barrier. Minor vomiting occurred in the infant until 1 week after delivery when the serum levels of lithium had fallen to below 0.2 mEq/1. 

Chloroprocaine (N,N -diethylaminoethyl 4-amino-2-chlorobenzoate) is a very short-acting, amino ester-type local anesthetic used to provide regional anesthesia by infiltration as well as by peripheral and central nerve block, including lumbar and caudal epidural blocks. The presence of a chlorine atom ortho to the carbonyl of the ester function increases its rate of hydrolysis by plasma cholinesterase at least threefold compared to procaine and benzocaine. Thus, chloroprocaine may be used in maternal and neonatal patients with minimal placental passage of chloroprocaine. The lower plasma cholinesterase activity in the maternal epidural space must still have sufficient activity for degrading chloroprocaine and, thus, not allowing it to cross the placenta barrier. 

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