Hoeldtke N J, Napolitano P G, Moore K H, Calhoun B C, Hume R F
Department of Obstetrics and Gynecology, Madigan Army Medical Center, Tacoma, Washington, USA.
Am J Obstet Gynecol. 1997 Nov;177(5):1088-92. doi: 10.1016/s0002-9378(97)70020-6.
Our purpose was to determine the effects of acidosis and acidosis-hypoxia on fetoplacental perfusion pressure and its response to angiotensin II.
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 x 10(-10) moles of angiotensin II. Fetoplacental perfusate was then replaced with either an acidotic medium (pH 6.90 to 7.00 and Po2 516 to 613 mm Hg) or an acidotic-hypoxic medium (pH 6.90 to 7.00 and Po2 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.
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).
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.
我们的目的是确定酸中毒和酸中毒 - 缺氧对胎儿 - 胎盘灌注压及其对血管紧张素II反应的影响。
对14个胎盘的灌注叶进行研究，其中7个使用酸中毒的胎儿循环灌注液，7个使用酸中毒 - 缺氧的胎儿循环灌注液。每个叶的胎儿血管系统最初在标准条件下灌注，并推注1×10⁻¹⁰摩尔的血管紧张素II。然后将胎儿 - 胎盘灌注液替换为酸性介质（pH 6.90至7.00，Po₂ 516至613 mmHg）或酸中毒 - 缺氧介质（pH 6.90至7.00，Po₂ 20至25 mmHg），随后注射血管紧张素II。随后用标准灌注液恢复血管系统，并再次注射血管紧张素II。通过单因素方差分析比较每组内的灌注压，结果以平均压力±标准误表示。
当胎儿循环灌注液变为酸性（28±1 mmHg对25±2 mmHg）或酸中毒 - 缺氧（26±2 mmHg对25±2 mmHg）时，静息胎儿 - 胎盘灌注压没有变化。对血管紧张素II反应所达到的最大胎儿 - 胎盘灌注压在酸性灌注液（41±2 mmHg对38±1 mmHg）或酸中毒 - 缺氧灌注液（39±2 mmHg对36±2 mmHg）之间没有差异。
在灌注的胎盘叶中，胎儿 - 胎盘灌注压和对血管紧张素II的升压反应不受胎儿循环酸中毒或酸中毒 - 缺氧的影响。这表明胎儿酸中毒或胎儿酸中毒合并缺氧均对胎儿 - 胎盘血管张力没有直接影响。
