Endothelin-1 constricts the feto-placental microcirculation and
decreases fetal oxygen consumption in sheep.
Adamson, S. L., Whiteley, K. J. and Langille, B. L.
Program in Development and Fetal Health, Samuel Lunenfeld Research
Institute, and Departments of Obstetrics and Gynecology, and
Pathology, University of Toronto, Mount Sinai Hospital, 600
University Avenue, Toronto, Canada, M5G 1X5
APStracts 2:0281H, 1995.
Endothelin-1 produced by umbilico-placental tissues may regulate fetal
placental perfusion. To investigate its site of action, we measured
segmental resistance in this bed in unanesthetized fetal sheep near
term during fetal endothelin-1 infusion. A 15 min i.v. infusion of
endothelin-1 at 1 [mu]g/min significantly increased fetal blood
pressure in the aorta (+33%), cotyledon artery and vein, and inferior
vena cava and decreased fetal heart rate (-40%). Vascular resistance
in the placental microcirculation increased significantly (+332%) but
smaller increases in resistance of the umbilical artery and vein were
not significant. Nevertheless, the stiffness of the umbilical
arterial wall appeared to increase because vascular input impedance
increased significantly both at the heart rate frequency (+85%) and
when averaged >2 Hz (characteristic impedance; +138%). Mean
blood flow in the umbilical artery decreased by 64% and the flow
pulsatility index increased 137% (P < 0.05 for both). Despite
the large decrease in placental perfusion, there was no significant
change in descending aortic oxygen tension or oxygen content because
fetal oxygen consumption was reduced by 40%. We conclude that
endothelin-1 is a potent constrictor of the placental
microcirculation in sheep. Endothelin-1 also decreases fetal oxygen
consumption by an unknown mechanism.
Received 23 March 1995; accepted in final form 27 June 1995.
APS Manuscript Number H278-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 11 July 1995.