Corticotropin-releasing hormone and cortisol in cord plasma in relation to gestational age, labor, and fetal distress.

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.