Adrenal Cortical Function in the Postmature Fetus and Newborn Infant

Abstract

Summaryumbilical cord, and evidence of fetal distress or anoxia. Stage 111 showed all the characteristics of the first two with evidence of The venous of d e h~-chronic asphyxia, a dirty yellow or yellow-green cord, and yellowdroepiandrosterone sulfate (DHAS), and unconjugated estriol stained nails and skin (2). Mortality was as high as 50% were compared in 54 37 POstterm9 and 22 POstmature in the acutely distressed stage I1 infants. Postmature newborns newborns. Pre-and postadrenocorticotropic hormone (ACTHI have twice the perinatal mortality as term babies (14), the stimulation levels of serum cortisol and DHAS were compared in overall postterm mortality rate at to 7% (13). Postmature newthe first t' days '' life in l9 postterm and '' POstmature borns are prone to develop hypoglycemia, asphyxic organ dysinfants. Comparison was also made between vaginally and cesar-function, and pulmonary aspiration syndrome. There is some can delivered postterm and postmature newborns. There evidence that postmature babies may have neurologic abnormalwere significantly greater cord blood cortisol levels in the post-ities which persist as learning disabilities when they reach school mature (260 * 22 n d m l (*S.E.)I, than in the normal (193 f 11 age (6).The possibility that the delayed onset of labor in pregnancies vaginally delivered infants. There were no significant differences a postmature fetus might be secondary to decreased fetal in the mean blood DHAS levels in the three groups (normal9 cortisol secretion was raised by Nwosu er al. (9, 10). They found *'" * POstterm9 U23 * nd* POstmature9that cortisol levels at 8 to 36 hr of age were lower in postmature d ) . Cortisol and DHAS responses to ACTHbabies than in their controls. Amniotic fluid analysis by the same were the same in the POstterm and POstmature groups. There was group, however, failed to demonstrate significantly lower cortisol a lower venous uncOnjugated estriO1 in the postmature than in the postterm babies (7). In spite of the level in the vaginally delivered postmature group (75 * 11 ndml) lower cortisol levels, a normal cortisol rise followed adreas compared in vagina'l~ delivered postterm * l4 noco~icotropic hormone (ACTH) administration in the postma-'dm' (' = 0'0')1 and * ndd ( ' < 0' *2)1 ture group (8). They concluded that there seemed to be no primary newborns. Stressed postmature infants cesarean set-adrenal insufficiency present in these babies, but that there was tion had higher uncOnjugated estriOl levels (83 * l2 than perhaps an inadequately functioning hypo~halamic-pituitary axis their unstressed, P s t t e m Cesarean section controls 140 * 9 n d (8). ln this study, we have examined function in ml (P < 0.01)1, but levels were still below those from vaginally postmature and postterm infants by measuring cortisol and dedelivered postterm infants. These findings substantiate normal hydroepiandrosterone sulfate (DHAS) before and after ACTH function in the fetus and newborn' stimulation. In addition, we have evaluated the function of the umbilical ve...

Estrogen upregulates cyclooxygenase-1 gene expression in ovine fetal pulmonary artery endothelium.

“…In a model of intrauterine infection induced with group B streptococcus in fetal rhesus monkeys, the normal rise in plasma estrogen which occurs before birth is absent (37). In addition, estrogen levels are greatly reduced in the cord blood of postmature human newborns (38). These observations suggest that in pregnancies complicated by placental dysfunction such as that associated with intrauterine infection or postmaturity, diminished estrogen synthesis by the placenta may lead to dimished fetal pulmonary COX-1 expression and impaired pulmonary PGI 2 synthesis, thereby contributing to the pathogenesis of persistent pulmonary hypertension of the newborn.…”

Effects of Antenatal Corticosteroids on Blood Pressure in Very Low Birth Weight Infants During the First 24 Hours of Life

“…26 Considerable evidence implicates the pituitary-adrenal axis and glucocorticoids as regulators of systemic BP in the preterm infant. [27][28][29][30][31][32] Glucocorticoids influence BP through several mechanisms: (1) increasing plasma and extracellular fluid by shifting fluid from the intracellular compartment, 29,30 (2) inducing the synthesis of angiotensinogen in hepatic cells, 33 (3) inhibiting the synthesis of vasodilator prostaglandins, 34,35 (4) increasing vascular responsiveness to ␣ adrenergic amines, 36,37 and (5) inhibiting nitric oxide production. 38 Preterm infants with hypotension that is resistant to vasopressors and volume expanders respond to relatively small doses of hydrocortisone.…”

Lipoprotein Utilization and Cholesterol Synthesis by the Human Fetal Adrenal Gland*

“…After birth, plasma DS levels fall precipitously and remain low through childhood until adrenarche, when the levels again rise (30). In contrast, during fetal life cortisol is secreted in smaller quantities as determined on the basis of its concentration in cord plasma (25,26,31) and as determined in in vitro studies of adrenal tissue during the first few days of culture (21)(22)(23)27). Although cortisol levels may increase slightly between early and late gestation (32), there is little evidence to suggest changes in cord plasma cortisol concentrations after 25 weeks until term, in contrast to DS levels (29,33).…”

“…The steroids secreted by the HFA gland are principally A 5 -sulfoconjugates, namely DS and pregnenolone sulfate (PS), as determined in studies of fetal adrenal tissue fragments during the first days of culture (21)(22)(23) and as estimated on the basis of the concentrations of these steroids in umbilical cord plasma (24)(25)(26). DS is the principal secretory product of the fetal zone, which comprises 80% of the total volume of the HFA gland.…”