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.