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Fetal cardiovascular reflex responses to hypoxaemia

Published online by Cambridge University Press:  10 October 2008

Dino A Giussani*
Affiliation:
University of College Medical School, London, UK.
John AD Spencer
Affiliation:
University of College Medical School, London, UK.
Mark A Hanson
Affiliation:
University of College Medical School, London, UK.
*Corresponding
Dr DA Giussani, Department of Obstetrics and Gynaecology, University College Medical School, 86–96 Chenies Mews, LondonWC1E 6HX.

Extract

The fetus mounts a coordinated cardiovascular response to an insult of acute hypoxaemia which involves neural and endocrine components. During acute hypoxaemia in late pregnancy there is a transient bradycardia, a gradual increase in arterial blood pressure and an increase in heart rate variability. In addition, there is a redistribution of the combined ventricular output favouring the cerebral, myocardial and adrenal circulations by shunting blood away from the peripheral circulations. A component of the increase in peripheral vascular resistance and the increase in arterial blood pressure during acute hypoxaemia is mediated via increases in plasma concentrations of vasoconstrictor hormones such as vasopressin, angiotensin II and neuropeptide Y. Whilst an increase in plasma ACTH and cortisol is also seen during acute hypoxaemia, their contribution to cardiovascular control in fetal sheep is less clear.

Evidence has been presented to suggest that a number of these cardiovascular and endocrine responses to acute hypoxaemia are chemorefiex in nature, mediated principally by carotid chemoreceptor afferents. In addition, this reflex may be modifiable in terms of changes in magnitude and gain: first, by an influence of the intrauterine environment during chronic hypoxaemia and second, through genetic influences, in animals adapted to life at high altitude.

Type
Articles
Copyright
Copyright © Cambridge University Press 1994

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