Fetoplacental vascular tone during fetal circuit acidosis and acidosis with hypoxia in the ex vivo perfused human placental cotyledon

• Published in: American journal of obstetrics and gynecology Vol. 177; no. 5; pp. 1088 - 1092
• Main Authors: Hoeldtke, Nathan J., Napolitano, Peter G., Moore, Katherine H., Calhoun, Byron C., Hume, Roderick F.
• Format: Journal Article Conference Proceeding
• Language: English
• Published: Philadelphia, PA Mosby, Inc 01.11.1997; Elsevier
• Subjects: Acidosis; Acidosis - physiopathology; angiotensin II; Angiotensin II - pharmacology; Biological and medical sciences; Blood Pressure; cotyledon; Diseases of mother, fetus and pregnancy; Female; Fetal Hypoxia - physiopathology; Fetus - blood supply; Gynecology. Andrology. Obstetrics; Humans; Hydrogen-Ion Concentration; hypoxia; Medical sciences; Nitric Oxide - physiology; Perfusion; Placenta - blood supply; Placenta - drug effects; placental perfusion; Pregnancy; Pregnancy. Fetus. Placenta; hypoxia; Acidosis; placental perfusion; angiotensin II; cotyledon; Human; Oxygen; Pregnancy disorders; Pathogenesis; Peptide hormone; Acid base balance disorder; Placenta diseases; In vitro; Fetal diseases; Renin angiotensin system; Metabolic disorder; Placenta; Ex vivo; Perfusion; Angiotensin; Fetus; Hypoxia; Blood pressure; Placental cotyledon
• ISSN: 0002-9378; 1097-6868
• DOI: 10.1016/S0002-9378(97)70020-6

Objectives: Our purpose was to determine the effects of acidosis and acidosis-hypoxia on fetoplacental perfusion pressure and its response to angiotensin II. Study Design: Perfused cotyledons from 14 placentas were studied with either an acidotic fetal circuit perfusate ( n = 7) or an acidotic-hypoxic fetal circuit perfusate ( n = 7). Each cotyledon's fetal vasculature was initially perfused under standard conditions and bolus injected with 1 × 10 –10 moles of angiotensin II. Fetoplacental perfusate was then replaced with either an acidotic medium (pH 6.90 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 injection. The vasculature was subsequently recovered with standard perfusate and again injected with angiotensin II. Perfusion pressures within each group were compared by one-way analysis of variance, and results were expressed as mean pressure ± SEM. Results: Resting fetoplacental perfusion pressure did not change when the fetal circuit perfusate was made acidotic (28 ± 1 mm Hg vs 25 ± 2 mm Hg) or acidotic-hypoxic (26 ± 2 mm Hg vs 25 ± 2 mm Hg). The maximal fetoplacental perfusion 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). Conclusions: In the perfused placental cotyledon fetoplacental perfusion pressure and pressor response to angiotensin II are not affected by fetal circuit acidosis or acidosis-hypoxia. This suggests that neither fetal acidosis nor fetal acidosis combined with hypoxia has a direct effect on fetoplacental vascular tone.