PLASMA BETA-ENDORPHIN CONCENTRATION IN DEPRESSED NEWBORNS AT TERM

Objective: The concentration of beta-endorphin in umbilical arterial b lood was related to plasma acid-base parameters, type of acidosis, and neonatal health immediately after delivery, to reveal whether fetal a cidosis and later, neonatal depression, were associated with elevated levels of beta-endorphin. Methods: Twenty-six, vaginally delivered inf ants, chosen at random, were studied. In 11 of 26 (42.3%) umbilical ar tery pH was under 7.20, and 6 of 26 (23.1%) were considered as having signs of neonatal depression, defined as a need for additional oxygena tion because of decreased respiratory drive at least during the first day of life. Arterial cord blood samples were collected at delivery fo r acid-base and beta-endorphin determinations. Neonatal acidosis, if p resent, was classified further as metabolic, respiratory, or mixed. Re sults: A significant positive correlation (r = 0.515, P = 0.0071) of b eta-endorphin and hydrogen ion ([H+]) concentration in fetal umbilical arterial blood was found in the group as a whole. In 11 acidotic chil dren (pH < 7.20, [H+] > 0.631 X 10(-7) mol/L), the umbilical artery be ta-endorphin concentration was 101.7 +/- 30.7 pmol/L (mean +/- SEM) wh ereas in 15 nonacidotic infants the respective beta-endorphin level wa s 18.6 +/- 4.8 pmol/L (P < 0.01). The concentration of plasma beta-end orphin was not dependent on the severity of acidosis, whether it was m etabolic, respiratory, or mixed. Six children with signs of neonatal r espiratory depression had significantly higher umbilical artery beta-e ndorphin value (111.4 +/- 39.5 pmol/L), whereas in healthy children (n = 20) the mean beta-endorphin concentration was 36.5 +/- 8.2 pmol/L ( P < 0.01). Compared with nondepressed acidotic infants, children with acidosis and depression had higher beta-endorphin levels, but the diff erence was not significant. Acid-base parameters were not found to dif fer significantly between the groups. Conclusions: Plasma beta-endorph in concentration in newborn umbilical artery at delivery might be cons idered as a consequence of fetal stress reaction during labor, with el evated levels in acidosis. It could be speculated that high beta-endor phin levels might prevent acidotic infants from getting rid of excess carbon dioxide, thus causing neonatal respiratory depression.