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Cortisol and ACTH responses to severe asphyxia in preterm fetal sheep
Author(s) -
Roelfsema Vincent,
Gunn Alistair J.,
Fraser Mhoyra,
Quaedackers Josine S.,
Bennet Laura
Publication year - 2005
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.2005.030320
Subject(s) - asphyxia , fetus , medicine , umbilical cord , endocrinology , hypoxia (environmental) , gestation , hydrocortisone , anesthesia , pregnancy , biology , chemistry , anatomy , oxygen , organic chemistry , genetics
It has been hypothesized that the hypothalamic‐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 days of gestation; term is 147 days), allocated to a sham control group ( 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 versus 14.1 ± 1.8 ng ml −1 in sham controls, 16‐fold) and cortisol levels (7.4 ± 4.9 versus 0.2 ± 0.1 ng ml −1 , 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.