Antenatal glucocorticoids alter premature newborn lamb neuroendocrine and endocrine responses to hypoxia

Citation
Mg. Ervin et al., Antenatal glucocorticoids alter premature newborn lamb neuroendocrine and endocrine responses to hypoxia, AM J P-REG, 279(3), 2000, pp. R830-R838
Citations number
44
Categorie Soggetti
Physiology
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY
ISSN journal
03636119 → ACNP
Volume
279
Issue
3
Year of publication
2000
Pages
R830 - R838
Database
ISI
SICI code
0363-6119(200009)279:3<R830:AGAPNL>2.0.ZU;2-8
Abstract
Glucocorticoids are administered for preterm labor to improve postnatal ada ptation. We assessed the effect of antenatal betamethasone (Beta) treatment on preterm newborn lamb neuroendocrine [catecholamine, arginine vasopressi n (AVP)] and endocrine [triiodothyronine (T-3), ANG II, and atrial natriure tic factor (ANF)] adaptive responses following delivery and a hypoxic chall enge. Beta treatment included direct fetal injection at 0.2 (F-0.2; n = 8) or 0.5 (F-0.5; n = 7) mg/kg estimated fetal body weight or maternal injecti on with 0.2 (n = 8) or 0.5 mg/kg (M-0.5; n = 8). Control animals received f etal and maternal intramuscular injections of saline (n = 8). After 24 h, l ambs were delivered by cesarean section, surfactant treated, and ventilated for 4 h. Relative to the control lambs, 3 h after delivery, there was a ma rked suppression of plasma cortisol, epinephrine, norepinephrine, and ANG I I levels and elevated plasma T-3 and ANF levels, systolic blood pressure, a nd left ventricular contractility (dP/dt; F-0.5 and M-0.5) values in F-0.5 and both maternal Beta-treated groups. However, Beta treatment augmented th e cardiac output, cortisol, norepinephrine, AVP, and ANF responses to 20 mi n of hypoxia (PO2 = 25-30 mmHg). We concluded that short-term (24 h) antena tal glucocorticoid exposure 1) alters preterm newborn postnatal blood press ure regulation in the face of marked depression of plasma cortisol, catecho lamine, and ANG II levels and 2) augments the postnatal neuroendocrine and endocrine responses to a hypoxic challenge.