Antenatal dexamethasone treatment decreases plasma catecholamine levels in preterm infants

被引:14
作者
Kallio, J
Karlsson, R
Toppari, J
Helminen, T
Scheinin, M
Kero, P
机构
[1] Univ Turku, Dept Pharmacol & Clin Pharmacol, FIN-20520 Turku, Finland
[2] Univ Turku, Dept Pediat, FIN-20520 Turku, Finland
[3] Univ Turku, Dept Physiol, FIN-20520 Turku, Finland
关键词
D O I
10.1203/00006450-199806000-00014
中图分类号
R72 [儿科学];
学科分类号
100202 ;
摘要
Antenatal corticosteroid therapy (ACT) has many beneficial effects on preterm infants. The cellular mechanisms of action of ACT include beta-adrenergic receptor-mediated cAMP generation. This study investigated the effects of ACT on sympathoadrenal mechanisms during immediate postnatal adaptation of preterm infants. Plasma epinephrine, norepinephrine, 3,4-dihydroxyphenylglycol, and cAMP were measured within 12 h after birth in 103 preterm infants (gestational age 24-36 wk), who were divided into two groups (non-ACT and ACT group) according to whether the mother had received dexamethasone treatment. Infants in the ACT group had significantly lower concentrations of plasma catecholamines than infants in the non-ACT group; plasma epinephrine was 38% lower, and plasma norepinephrine was 20-40% lower in the ACT group, depending on gestational age (r = -0.37 in the nan-ACT group and r = -0.28 in the ACT group, p < 0.05. Plasma cAMP concentrations were similar in the two groups. Antihypertensive treatment of the mother was associated with low plasma cAMP (p < 0.001), whereas tocolytic treatment was associated with high plasma cAMP (p = 0.001) of the infant. The results indicate that ACT attenuates the birth-related increase in plasma catecholamines. Still, plasma cAMP levels remain high, which suggests enhanced beta-adrenoceptor signaling after ACT.
引用
收藏
页码:801 / 807
页数:7
相关论文
共 43 条
[21]   PRENATAL DEXAMETHASONE EXPOSURE CAUSES LOSS OF NEONATAL HYPOXIA TOLERANCE - CELLULAR MECHANISMS [J].
KAUFFMAN, KS ;
SEIDLER, FJ ;
SLOTKIN, TA .
PEDIATRIC RESEARCH, 1994, 35 (05) :515-522
[22]   GLUCOCORTICOID REGULATION OF G-PROTEIN SUBUNITS IN NEONATAL LIVER [J].
KAWAI, Y ;
ARINZE, IJ .
MOLECULAR AND CELLULAR ENDOCRINOLOGY, 1993, 90 (02) :203-209
[23]   URINARY ADENOSINE-3',5'-MONOPHOSPHATE EXCRETION IN CHILDHOOD [J].
KRUSE, K ;
KRACHT, U .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1981, 53 (06) :1251-1255
[24]  
KUDLACZ EM, 1990, J DEV PHYSIOL, V14, P273
[25]   HORMONAL-REGULATION OF POTASSIUM SHIFTS DURING GRADED EXHAUSTING EXERCISE [J].
LASO, FJ ;
GONZALEZBUITRAGO, JM ;
RUIZ, CM ;
DECASTRO, S .
EUROPEAN JOURNAL OF APPLIED PHYSIOLOGY AND OCCUPATIONAL PHYSIOLOGY, 1991, 62 (04) :292-296
[26]  
LAU C, 1981, J PHARMACOL EXP THER, V216, P6
[27]  
LEVITON A, 1993, PEDIATRICS, V91, P1083
[28]   AN EXPLORATION OF OPINION AND PRACTICE PATTERNS AFFECTING LOW USE OF ANTENATAL CORTICOSTEROIDS [J].
LEVITON, LC ;
BAKER, S ;
HASSOL, A ;
GOLDENBERG, RL .
AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY, 1995, 173 (01) :312-316
[29]  
MAIER JA, 1989, J DEV PHYSIOL, V12, P249
[30]   PERMISSIVE HORMONE REGULATION OF HORMONE-SENSITIVE EFFECTOR SYSTEMS [J].
MALBON, CC ;
RAPIEJKO, PJ ;
WATKINS, DC .
TRENDS IN PHARMACOLOGICAL SCIENCES, 1988, 9 (01) :33-36