ABSTRACT
Concentration of corticotropin-releasing hormone (CRH) has earlier been found to increase
greatly in maternal plasma during the last trimester of normal pregnancy and even
more in preeclampsia. This CRH is thought to be of placental origin, and it may stimulate
maternal or fetal pituitary adrenal axis. We studied CRH in umbilical cord venous
plasma in relation to gestation, labor, and fetal distress. There was a great maternal-to-fetal
concentration difference in plasma CRH levels, a hundredfold at term pregnancy, suggesting
that the placenta releases CRH mainly into the maternal rather than into the fetal
circulation. Length of gestation or the mode of delivery did not affect CRH levels
in cord plasma. Cord CRH levels were higher (median, 24.1, range, 14.2 to 67 pmol/liter)
in six preterm infants with chronic fetal distress, born to mothers with severe preeclampsia
and in nine infants born after premature rupture of membranes (median, 17.0, range,
7.65 to 53 pmol/liter), than in 12 preterm control infants born after uncomplicated
pregnancy (median, 6.3 range, 1.0 to 27.5 pmol/liter). No significant correlation
was found between CRH and Cortisol levels in cord plasma. Increased Cortisol levels
in cord plasma were associated with spontaneous vaginal delivery but not with chronic
fetal distress. These findings demonstrated that placental release of CRH into the
fetal circulation may be increased in pregnancy complications with chronic fetal distress
but failed to prove any relationship between placental CRH and fetal adrenal function.
