Maternal beta-adrenergic tocolysis and neonatal bilirubin production.
The potential for beta-adrenergic drugs to increase total bilirubin formation via cyclic adenosine monophosphate-mediated stimulation of hepatic microsomal heme oxygenase in the human neonate was evaluated. The pulmonary excretion rate of endogenously produced carbon monoxide (VeCO), an index of total bilirubin formation (TBF), was measured in 18 preterm neonates whose mothers received beta-adrenergic drugs for tocolysis and in 18 preterm neonates whose mothers were untreated. The mean VeCO of the neonates in the former group (17.2 +/- 7.3 microL/kg/hr) was the same as that in the latter group (17.4 +/- 6.2 microL/kg/hr); both values were elevated when compared with the mean VeCO of 20 term newborns (13.9 +/- 3.5 microL/kg/hr). Our findings indicate that TBF is not significantly increased in neonates whose mothers received beta-adrenergic drugs before delivery.
D000318:Adrenergic beta-Agonists / Q000494:pharmacology* / Q000627:therapeutic use; D001663:Bilirubin / Q000096:biosynthesis*; D002248:Carbon Monoxide / Q000032:analysis / Q000502:physiology; D005260:Female; D006801:Humans; D007231:Infant, Newborn; D007234:Infant, Premature; D007752:Obstetric Labor, Premature / Q000517:prevention & control*; D011247:Pregnancy; D012312:Ritodrine / Q000494:pharmacology / Q000627:therapeutic use; D013726:Terbutaline / Q000494:pharmacology / Q000627:therapeutic use
D000318:Adrenergic beta-Agonists; D002248:Carbon Monoxide; D012312:Ritodrine; D013726:Terbutaline; D001663:Bilirubin