Placenta - continued

After the corpus luteum dies, the placenta continues to produce large amounts of progesterone. 

Rh incompatibility may occur when an Rh negative mother carries an Rh-positive fetus. At the time of delivery, a small amount of the baby s Rh-positive blood may gain access to the maternal circulation. In response, the immune system of the mother produces anti-Rh antibodies. During the subsequent pregnancy, the fetus is exposed to these antibodies as they cross the placenta. If this fetus is also Rh-positive, then the anti-Rh antibodies attack the fetal erythrocytes and cause hemolytic disease of the newborn (erythroblastosis fetalis). This may occur in about 3% of second Rh-positive babies and about 10% of third Rh-positive babies. The incidence continues to increase with subsequent pregnancies. 

The kidney begins to function as soon as there are functional nephrons at the corticomedullary junction. Nephron development continues during this time in the periphery of the cortex. Production of urine starts at about the end of the 3rd month in humans and by gestation day 17 or 18 in rats. Urine production is not necessary for waste excretion from the fetus, as this is taken care of by the placenta. Urine production is necessary to maintain proper amniotic fluid volume. Fetuses without kidneys or with insufficient urine production have oligohydramnios, too little amniotic fluid. Oligohydramnios can lead to abnormal development by physically confining the fetus, sometimes resulting in amputation or deformation of limbs in utero. 

Maternal and fetal outcomes have been investigated when insulin lispro has been used during pregnancy [Radermecker 178]. Insulin lispro is unlikely to cross the placenta when used in a single standard dose. Lispro was not found in the cord blood of neonates whose mothers had received a continuous intravenous infusion of lispro. These data and data from controlled studies showing similar outcomes in women treated with conventional insulin are reassuring. 

Much has been said about the positive effects of vitamin E (a-tocopherol) on sexual performance and ability in humans. Unfortunately, there is little scientific rationale to substantiate such claims. The primary reasons for attributing a positive role in sexual performance to vitamin E come from experiments on vitamin E deficiency in laboratory animals. In such experiments the principal manifestation of this deficiency is infertility, although the reasons for this condition differ in males and females. In female rats there is no loss in ability to produce apparently healthy ova, nor is there any defect in the placenta or uterus. However, fetal death occurs shortly after the first week of embryonic life, and fetuses are reabsorbed. This situation can be prevented if vitamin E is administered any time up to day 5 or 6 of embryonic life. In the male rat the earliest observable effect of vitamin E deficiency is immobility of spermatozoa, with subsequent degeneration of the germinal epithelium. Secondary sex organs are not altered and sexual vigor is not diminished, but vigor may decrease if the deficiency continues. 

Human placenta BBV Miyamoto et al. (1988). FEBS Lett. 231,263-267. (continued)... 

Pregnancy. If a pregnant woman has hyperthyroidism (2/1000 pregnancies) she should be treated with the smallest possible amount of these drugs because they cross the placenta with overtreatment fetal goitre occurs. Surgery in the second trimester may be preferred to continued drug therapy. 

Pregnant colitic patients generally fare better if they continued to take aminosalicylates. Though sulfasalazine crosses the placenta, competes for albumin-binding sites with bilirubin, and can be detected in breast milk, no adverse effects on offspring have been detected. 

Enalapril, captopril, and lisinopril (and presumably other ACE inhibitors) cross the placenta in pharmacologically significant amounts (17). There is clear evidence of fetotoxicity when ACE inhibitors are used beyond the first trimester of pregnancy. Since continuation of treatment beyond the first trimester carries an excess risk of low fetal birth weight and other more severe complications, it is important to withdraw the ACE inhibitor at this time. Intrauterine growth retardation, oligohydramnios, and neonatal renal impairment, often with a serious outcome, are characteristic (98) failure of ossification of the skuU or hypocalvaria also appear to be part of the pattern (17). There is also evidence that persistence of a patent ductus arteriosus is also more likely to occur. 

The pharmacological actions of hCG are essentially the same as those of LH. In females during pregnancy, the hCG secreted by the placenta maintains the corpus luteum to continue secretion of estrogen and progesterone, thus inhibiting ovulation and menstruation. 

Propofol Propofol has been relatively free of acute side effects other than those associated with its mechanism of action. Continuous infusions lasting greater than 10 days in ICUs have demonstrated no significant apparent toxicities. Propofol is not recommended for obstetrics, including cesarean section deliveries. It crosses the placenta, and as with other general anesthetic agents, may be associated with neonatal depression. Propofol is not recommended for use in nursing mothers because it is excreted in human milk, and the effects of oral absorption of small amounts of propofol in newborn and infants are not known. 

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