beta-endorphin and Infant--Premature--Diseases

Apnea of prematurity is a common problem in neonatal intensive care nurseries. Xanthines are used to treat apnea, but their mechanism of action is not clearly understood. To determine whether xanthines stimulated beta-endorphin (beta-ED) release in preterm infants, plasma beta-ED concentrations were measured in 27 infants with apnea of prematurity. These infants had a mean (+/- SD) birthweight of 1560 +/- 487 g, gestational age 31 +/- 2.5 weeks, and a postnatal age of 7.3 +/- 4.6 d. Twenty-five of the infants were treated with I.V. aminophylline 2.5 mg/kg/dose 4 times daily and 2 were treated orally with caffeine (10 mg/kg). Blood samples were collected prior to and 30 min after treatment with xanthines. Apneic spells greater than 15 sec were recorded and reviewed every 24 h using a Hewlett-Packard Merlin Monitor (Waltham, MA.) system. Infants were then stratified into responders (Group 1, n = 14) and nonresponders (Group 2, n = 13), with responders defined as showing more than 50% decrease in the frequency of apneic spells in the first 24 h of treatment. beta-ED were measured as previously described using a radioimmunoassay technique. In group 1, plasma beta-ED concentration increased significantly, (p = 0.0496) from pre-xanthine (24.4 +/- 12 pg/ml) to post xanthine (34.6 +/- 24 pg/ml) treatment, whereas in Group 2 the concentrations remained the same (23.3 +/- 5 pg/ml) and (22.6 +/- 4 pg/ml). Birthweight, gestational age, postnatal age, and diagnoses in both groups were compared and no significant differences were observed. Interestingly, xanthine treatment caused increased plasma beta-ED release when apneas decreased.

Topics: Apnea; beta-Endorphin; Caffeine; Humans; Infant, Newborn; Infant, Premature, Diseases; Xanthine; Xanthines

Twenty-nine premature infants were studied to determine whether neonatal asphyxia, apnea, and low blood pressure in the first day of life are associated with elevated plasma beta-endorphin concentrations. Plasma beta-endorphin levels were determined at 0.5 to 2, 4 to 6, and 18 to 24 hours of life, using radioimmunoassay. Premature infants with moderate or severe asphyxia (n = 19) had higher levels at 0.5 to 2 hours of age (32.1 +/- 6.7 vs 16.4 +/- 7.4 pmol/L) and significantly higher levels at 4 to 6 hours of age (50.4 +/- 10.0 vs 22.9 +/- 9.2 pmol/L) compared with the ten nonasphyxiated premature infants. A significant elevation in levels at age 0.5 to 2 hours (39.4 +/- 9.9 vs 17.7 +/- 4.4 pmol/L) and age 4 to 6 hours (59.3 +/- 13.8 vs 27.1 +/- 17.1 pmol/L) was observed in premature infants with low blood pressure or impaired perfusion (n = 12) who required the administration of volume expanders. No differences were observed in premature infants with and without apnea. It may be speculated that the increased endogenous release of beta-endorphins in response to perinatal asphyxia may play a role in the pathogenesis of shock observed in the first day of life.

Topics: Apnea; Asphyxia Neonatorum; beta-Endorphin; Endorphins; Humans; Hypotension; Infant, Low Birth Weight; Infant, Newborn; Infant, Premature, Diseases; Radioimmunoassay

In an attempt to determine whether plasma beta-endorphin (beta-ED) concentrations correlate with occurrence of apnea in preterm infants, measurements were made in three groups of infants. The control group consisted of 11 infants with a mean (+/- SEM) gestational age of 30.5 +/- 0.8 weeks, a mean (+/- SEM) birthweight of 1650 +/- 180 g, and a mean (+/- SEM) postnatal age of 1.3 +/- 0.5 days. Eight infants with apnea, bradycardia, and associated hypotension had a mean (+/- SEM) gestational age, birthweight and postnatal age of 30 +/- 0.9 weeks, 1165 +/- 90 g, and 7.8 +/- 1.9 days, respectively. The third group consisted of eight infants experiencing apnea alone without bradycardia and had a mean (+/- SEM) gestational age, birthweight, and postnatal age of 31 +/- 0.8 weeks, 1380 +/- 125 g, and 2.6 +/- 0.9 days, respectively. The last two groups of infants suffered varying degrees of apnea, but differed in their severity. The plasma endorphin concentrations (+/- SEM) were 26.9 +/- 2, 68.0 +/- 9.0, and 39.6 +/- 2.0 pg/ml, respectively, for the previously described three groups. Significant elevation in beta-ED concentration was observed in the severely apneic infants with bradycardia when compared to the other two groups. The association of increased plasma beta-ED release with severe apneic spells may suggest that these endogenous opiates play a role in the pathophysiology of apnea of prematurity.

Topics: Apnea; beta-Endorphin; Bradycardia; Endorphins; Humans; Hypotension; Infant, Newborn; Infant, Premature, Diseases; Radioimmunoassay; Recurrence

Topics: Apnea; beta-Endorphin; Endorphins; Humans; Infant, Newborn; Infant, Newborn, Diseases; Infant, Premature, Diseases