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RESEARCH ARTICLE
Contents Vol 16(6)

Effect of graded hypoxia on activin A, prostaglandin E2 and cortisol levels in the late-pregnant sheep

V. G. Supramaniam A D , G. Jenkin A , E. M. Wallace B , A. E. O’Connor C , D. M. de Kretser C and S. L. Miller A
+ Author Affiliations
- Author Affiliations

A Department of Physiology, Building 13F, Monash University, Victoria 3800, Australia.

B Department of Obstetrics and Gynaecology, Monash University, Victoria 3800, Australia.

C Institute of Reproduction and Development, Monash University, Clayton, Victoria 3168, Australia.

D To whom correspondence should be addressed. email: veena.supramaniam@med.monash.edu.au

Reproduction, Fertility and Development 16(6) 625-632 https://doi.org/10.1071/RD03110
Submitted: 23 December 2003  Accepted: 10 May 2004   Published: 16 August 2004

Abstract

The aim of the present study was to determine whether activin A concentrations are dependent on feto–placental oxygen availability and to investigate the temporal relationship of activin A with prostaglandin (PG) E2 and cortisol. Nine fetal sheep (six hypoxic and three control) were instrumented and catheterised at 0.8 gestation. Reduced uterine blood flow was used to achieve three levels of hypoxia (mild = fetal SaO2 40–50%; moderate = fetal SaO2 30–40%; severe = fetal SaO2 20–30%), for 4 h on 3 consecutive days. Activin A, PGE2 and cortisol levels were determined in maternal and fetal blood and amniotic fluid. Moderate and severe hypoxia produced a significant (P < 0.05) increase in fetal plasma activin A concentrations. The amniotic fluid activin A concentrations were 15-fold higher than those in the fetal circulation, but were unchanged by hypoxia. The fetal PGE2 response reflected the degree of hypoxia over the 3 days, with moderate and severe hypoxia producing a significant (P < 0.05) increase in PGE2 concentrations. Fetal plasma cortisol concentrations were increased (P < 0.05) during all levels of hypoxia. Fetal arterial activin A was increased in response to moderate and severe hypoxia, but levels were not maintained over the hypoxic period. The increases in activin A and cortisol concentrations preceded the increase in PGE2.


Acknowledgments

We thank Jan Loose for technical support and Alex Satragno and Stuart Hooper for assistance with the preparation of animals. This work was supported by a National Health and Medical Research Council of Australia Program Grant to G. Jenkin and D. de Kretser.


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