FETOPLACENTAL VASCULAR TONE DURING FETAL CIRCUIT ACIDOSIS AND ACIDOSIS WITH HYPOXIA IN THE EX-VIVO PERFUSED HUMAN PLACENTAL COTYLEDON

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.