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