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

Author:

Ervin M. Gore1,Padbury James F.2,Polk Daniel H.3,Ikegami Machiko4,Berry Lynne M.5,Jobe Alan H.4

Affiliation:

1. Department of Biology, Middle Tennessee State University, Murfreesboro, Tennessee 37132;

2. Department of Pediatrics, Women's and Infants Hospital of Rhode Island, Brown University, Providence, Rhode Island 02905;

3. Children's Memorial Hospital, Northwestern University Medical School, Chicago, Illinois 60614;

4. Children's Hospital Medical Center, Division of Pulmonary Biology, Cincinnati, Ohio 45229; and

5. Perinatal Research Laboratories, Department of Pediatrics, University of California, Los Angeles School of Medicine, Harbor-University of California Los Angeles Medical Center, Torrance, California 90502

Abstract

Glucocorticoids are administered for preterm labor to improve postnatal adaptation. We assessed the effect of antenatal betamethasone (Beta) treatment on preterm newborn lamb neuroendocrine [catecholamine, arginine vasopressin (AVP)] and endocrine [triiodothyronine (T3), ANG II, and atrial natriuretic factor (ANF)] adaptive responses following delivery and a hypoxic challenge. Beta treatment included direct fetal injection at 0.2 (F0.2; n = 8) or 0.5 (F0.5; n = 7) mg/kg estimated fetal body weight or maternal injection with 0.2 ( n = 8) or 0.5 mg/kg (M0.5; n = 8). Control animals received fetal and maternal intramuscular injections of saline ( n = 8). After 24 h, lambs were delivered by cesarean section, surfactant treated, and ventilated for 4 h. Relative to the control lambs, 3 h after delivery, there was a marked suppression of plasma cortisol, epinephrine, norepinephrine, and ANG II levels and elevated plasma T3 and ANF levels, systolic blood pressure, and left ventricular contractility (dP/d t; F0.5 and M0.5) values in F0.5 and both maternal Beta-treated groups. However, Beta treatment augmented the cardiac output, cortisol, norepinephrine, AVP, and ANF responses to 20 min of hypoxia (Po 2 = 25–30 mmHg). We concluded that short-term (24 h) antenatal glucocorticoid exposure 1) alters preterm newborn postnatal blood pressure regulation in the face of marked depression of plasma cortisol, catecholamine, and ANG II levels and 2) augments the postnatal neuroendocrine and endocrine responses to a hypoxic challenge.

Publisher

American Physiological Society

Subject

Physiology (medical),Physiology

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