Nj. Hoeldtke et al., FETOPLACENTAL VASCULAR TONE DURING FETAL CIRCUIT ACIDOSIS AND ACIDOSIS WITH HYPOXIA IN THE EX-VIVO PERFUSED HUMAN PLACENTAL COTYLEDON, American journal of obstetrics and gynecology, 177(5), 1997, pp. 1088-1092
OBJECTIVES: Our purpose was to determine the effects of acidosis and a
cidosis-hypoxia on fetoplacental perfusion pressure and its response t
o angiotensin II. STUDY DESIGN: Perfused cotyledons from 14 placentas
were studied with either an acidotic fetal circuit perfusate (n = 7) o
r an acidotic-hypoxic fetal circuit perfusate (n = 7). Each cotyledon'
s fetal vasculature was initially perfused under standard conditions a
nd bolus injected with 1 x 10(-10) moles of angiotensin II. Fetoplacen
tal perfusate was then replaced with either an acidotic medium (pH 6.9
0 to 7.00 and Po-2 516 to 613 mm Hg) or an acidotic-hypoxic medium (pH
6.90 to 7.00 and Po-2 20 to 25 mm Hg) followed by an angiotensin II i
njection. The vasculature was subsequently recovered with standard per
fusate and again injected with angiotensin II. Perfusion pressures wit
hin each group were compared by one-way analysis of variance, and resu
lts were expressed as mean pressure +/- SEM. RESULTS: Resting fetoplac
ental perfusion pressure did not change when the fetal circuit perfusa
te was made acidotic (28 +/- 1 mm Hg vs 25 +/- 2 mm Hg) or acidotic-hy
poxic (26 +/- 2 mm Hg vs 25 +/- 2 mm Hg). The maximal fetoplacental pe
rfusion pressure achieved in response to angiotensin ii did not differ
with an acidotic perfusate (41 +/- 2 mm Hg vs 38 +/- 1 mm Hg) or with
an acidotic-hypoxic perfusate (39 +/- 2 mm Hg vs 36 +/- 2 mm Hg). CON
CLUSIONS: In the perfused placental cotyledon fetoplacental perfusion
pressure and presser response to angiotensin II are not affected by fe
tal circuit acidosis or acidosis-hypoxia. This suggests that neither f
etal acidosis nor fetal acidosis combined with hypoxia has a direct ef
fect on fetoplacental vascular tone.