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HYPOXIA-REOXYGENATION; A POTENTIAL SOURCE OF PLACENTAL OXIDATIVE STRESS IN NORMAL PREGNANCY AND PREECLAMPSIA

Published online by Cambridge University Press:  08 July 2003

GRAHAM J BURTON
Affiliation:
Department of Anatomy, University of Cambridge, Cambridge
TAI-HO HUNG
Affiliation:
Department of Anatomy, University of Cambridge, Cambridge Department of Obstetrics and Gynaecology, Chang Gung Memorial Hospital, Taipei, Taiwan

Extract

It is now over half a century since Arthur Hertig first reported vascular pathology in the uterine arteries supplying the placenta in women suffering from preeclampsia. His pioneering histological studies have been validated and extended by many others, leading to the general concept that placental perfusion is compromised in these patients. More recent Doppler ultrasound studies have confirmed reduced intervillous blood flow in vivo, and so gradually a consensus has emerged that the placental lesions associated with preeclampsia arise from a state of chronic hypoxia. Whilst hypoxia may undoubtedly play a significant role in the generation of placental pathology, there is considerable evidence that another feature of the intervillous circulation, namely the constancy of the blood flow, may be a more important factor. In this review we propose that hypoxia-reoxygenation, secondary to intermittent perfusion of the intervillous space, is a more physiological approach to take to understanding the pathophysiology of both normal pregnancies, and those complicated by preeclampsia. We further propose that chronic reduction in placental perfusion alone may lead to fetal growth restriction, and that if the two phenomena are superimposed then preeclampsia with growth restriction will result.

Type
Research Article
Copyright
© Cambridge University Press 2003

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HYPOXIA-REOXYGENATION; A POTENTIAL SOURCE OF PLACENTAL OXIDATIVE STRESS IN NORMAL PREGNANCY AND PREECLAMPSIA
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HYPOXIA-REOXYGENATION; A POTENTIAL SOURCE OF PLACENTAL OXIDATIVE STRESS IN NORMAL PREGNANCY AND PREECLAMPSIA
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HYPOXIA-REOXYGENATION; A POTENTIAL SOURCE OF PLACENTAL OXIDATIVE STRESS IN NORMAL PREGNANCY AND PREECLAMPSIA
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