K. Sankaran et al., PLASMA BETA-ENDORPHIN CONCENTRATION AND XANTHINE TREATMENT IN APNEA OF PREMATURITY, Clinical and investigative medicine, 16(3), 1993, pp. 197-203
Apnea of prematurity is a common problem in neonatal intensive care nu
rseries. Xanthines are used to treat apnea, but their mechanism of act
ion is not clearly understood. To determine whether xanthines stimulat
ed 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, gesta
tional age 31 +/- 2.5 weeks, and a postnatal age of 7.3 +/- 4.6 d. Twe
nty-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 wit
h xanthines. Apneic spells greater than 15 sec were recorded and revie
wed every 24 h using a Hewlett-Packard Merlin Monitor (Waltham, MA.) s
ystem. Infants were then stratified into responders (Group 1, n = 14)
and nonresponders (Group 2, n = 13), with responders defined as showin
g more than 50% decrease in the frequency of apneic spells in the firs
t 24 h of treatment. Beta-ED were measured as previously described usi
ng a radioimmunoassay technique. In group 1, plasma beta-ED concentrat
ion increased significantly, (p = 0.0496) from pre-xanthine (24.4 +/-
12 pg/ml) to post xanthine (34.6 +/- 24 pg/ml) treatment, whereas in G
roup 2 the concentrations remained the same (23.3 +/- 5 pg/ml) and (22
.6 +/- 4 pg/ml). Birthweight, gestational age, postnatal age, and diag
noses in both groups were compared and no significant differences were
observed. Interestingly, xanthine treatment caused increased plasma b
eta-ED release when apneas decreased.