Hypoxic-ischemic encephalopathy and plasma beta-endorphin.

In an attempt to determine whether hypoxic-ischemic encephalopathy in and of itself or its associated pathologic conditions lead to increased concentrations of plasma beta-endorphin (beta-ED), measurements were made in three groups of term infants. Group 1 (control) consisted of 8 infants with a mean gestation of 38.6 +/- (SE) 0.4 weeks, a mean birth weight of 3,420 +/- 150 g, and a mean postnatal age of 1.4 +/- 0.7 days. Group 2 consisted of 10 infants with a mean gestational age, birth weight and postnatal age of 40.1 +/- 0.5 weeks, 3,310 +/- 80 g and 3,9 +/- 1.1 days, and group 3 included 6 infants with a mean gestational age, birth weight and postnatal age of 40.4 +/- 1 weeks, 3,650 +/- 310 g, and 2.8 +/- 1 days, respectively. The group 2 and 3 infants suffered clinical and neurological evidence of hypoxic-ischemic brain injury from perinatal asphyxia; however, the infants in group 2 suffered additional problems such as meconium aspiration, persistent fetal circulation with ongoing hypoxemia as measured by transcutaneous or umbilical arterial oxygen monitoring. The group 3 infants were normoxemic after resuscitation. The mean plasma beta-ED concentrations were 19 +/- (SE) 2.7, 103 +/- 35.7 and 25 +/- 4.5 pg/ml in groups 1, 2 and 3, respectively. A significant elevation of plasma beta-ED concentration was observed in group 2 when compared to groups 1 and 3. The association of increased plasma beta-ED concentration in infants with hypoxic-ischemic encephalopathy associated with ongoing hypoxemia suggests that hypoxemia may act as a strong stimulus for plasma beta-ED release in term infants.