Received February 20, 2005
Revised March 4, 2005
Accepted after revision March 4, 2005
Neuroendocrinology/endocrinology
|
Cortisol and ACTH responses to severe asphyxia in preterm fetal sheep
Vincent Roelfsema 1,
Alistair Jan Gunn 1*,
Mhoyra Fraser 1,
Josine S. Quaedackers 1,
Laura Bennet 1
1 University of Auckland
* To whom correspondence should be addressed. E-mail: aj.gunn{at}auckland.ac.nz.
 |
Abstract |
|---|
It has been hypothesized that the hypothalamus-pituitary-adrenal (HPA) axis is immature in the preterm fetus and that this compromises their ability to adapt to hypoxic stress; however, there are few direct data. We therefore examined the effects of asphyxia on HPA responses in chronically instrumented preterm fetal sheep (104 d of gestation, term is 147 d), allocated to sham control (n=7) or 25 min of complete umbilical cord occlusion (n=8), followed by recovery for 72 h. During umbilical cord occlusion there was a rapid rise in ACTH levels (230.4±63.5 vs. 14.1±1.8 ng/ml in sham controls, 16 fold) and cortisol levels (7.4±4.9 vs. 0.2±0.1 ng/ml, 31 fold), with further increases after release of cord occlusion. ACTH levels were normalized by 24 h, while plasma cortisol levels returned to sham control values 72 h after asphyxia. Fetal arterial blood pressure was elevated in the first 36 h, with a marked increase in femoral vascular resistance, and correlated positively with cortisol levels after asphyxia (P=0.05). In conclusion, the preterm fetus shows a brisk, substantial HPA response to severe hypoxia.
Key Words:
Adrenocorticotrophic hormone (ACTH), Fetal, Hypoxia
