Chronic fetal placental embolization and hypoxemia causes hypertension and myocardial hypertrophy in fetal sheep. Murotsuki, Jun, John R. G. Challis, Victor K. M. Han, Laurence J. Fraher, and Robert Gagnon. Medical Research Council Group in Fetal and Neonatal Health and Development, Departments of Obstetrics and Gynaecology, Physiology, Paediatrics, Biochemistry, Anatomy, and Medicine, University of Western Ontario, and Lawson Research Institute, St. Joseph's Health Centre, London, Ontario, N6A 4V2; and Department of Physiology, University of Toronto, Toronto, Ontario, M5S 1A8 Canada
APStracts 3:0289R, 1996.
To examine the cardiovascular effects on the fetus of an elevated umbilical vascular resistance resulting in fetal hypoxemia, we embolized the fetal side of the placenta in pregnant sheep and measured cardiovascular and hormonal changes and cellular growth in fetal heart. Chronically catheterized fetal sheep were embolized (n=6) for 21 days between 0.74 and 0.88 of gestation into the descending aorta, until arterial oxygen content was decreased by 40 -50% of the pre-embolization value. Control animals (n=6) received saline only. During embolization, fetuses became chronically hypoxemic (p&LT0.001) and hypertensive (p&LT0.001) with a progressive increase in umbilical artery resistance index (p&LT0.001). There was also an increase in fetal plasma norepinephrine throughout the study period (p&LT0.05). On day 21 of embolization, fetuses showed asymmetrical growth restriction, increased heart weight (p&LT0.01) and increase in right and left ventricular wall thickness (p&LT0.05) compared with control animals. The protein/DNA ratio, an index of cell size, increased in the right ventricular myocardium in the embolized group (p&LT0.001), suggesting myocardial cell hypertrophy. We conclude that during chronic placental damage that caused fetal hypoxemia with an increase in umbilical artery resistance index, fetuses developed arterial hypertension and asymmetrical growth restriction, and that increases in afterload to the heart and plasma norepinephrine likely caused fetal myocardial hypertrophy.

Received 26 March 1996; accepted in final form 9 July 1996.
APS Manuscript Number R179-6.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 4 August 1996