Gagnon R, Johnston L, Murotsuki J
Department of Obstetrics and Gynaecology, St. Joseph's Health Centre, London, Ontario, Canada.
Am J Obstet Gynecol. 1996 Jul;175(1):63-72. doi: 10.1016/s0002-9378(96)70252-1.
Our goal was to determine the effect of chronic and acute umbilical-placental embolization on placental hemodynamic and fetal heart rate patterns in relation to fetal oxygenation in the near-term ovine fetus.
Daily fetal placental embolization was performed during 10 days in 9 sheep fetuses until fetal arterial oxygen content decreased by approximately 30%. Nine control fetuses received saline solution. Mean and pulsatile umbilical blood flow, perfusion pressure, placental vascular resistance, fundamental impedance, pressure pulsatility index, and umbilical artery resistance index corrected to a fetal heart rate of 160 beats/min were measured. On day 10 both groups were acutely embolized until fetal arterial pH decreased to approximately 7.00. Fetal heart rate was measured with the Sonicaid System 8000 (Oxford Sonicaid, Oxford, United Kingdom).
Chronic fetal placental embolization was associated with a progressive reduction in umbilical blood flow (p < 0.00001) and fetal arterial oxygen content (p < 0.001) whereas fetal heart rate patterns remained unaltered. A chronic increase in umbilical artery resistance index corrected to a fetal heart rate of 160 beats/min could be entirely explained only if the changes in umbilical artery pressure pulsatility index and the fundamental impedance were taken into account, in addition to the changes observed in placental vascular resistance. During acute embolization leading to a 50% reduction in umbilical blood flow (p < 0.0002) and a three times increase in placental vascular resistance (p < 0.0001), the most consistent change in fetal heart rate patterns related to progressive metabolic acidosis was an 84% decrease in absolute acceleration frequency (p < 0.0001) whereas short-term fetal heart rate variability remained unaltered.
Changes in umbilical artery resistance index induced by chronic umbilical-placental embolization resulting in fetal hypoxemia occurred before any changes in fetal heart rate patterns were detectable. A decrease in the absolute acceleration frequency was the only component of fetal heart rate patterns related to progressive metabolic acidosis in the near-term ovine fetus.
我们的目标是确定慢性和急性脐-胎盘栓塞对近足月绵羊胎儿胎盘血流动力学和胎儿心率模式的影响，并探讨其与胎儿氧合的关系。
对9只绵羊胎儿在10天内每天进行胎儿胎盘栓塞，直至胎儿动脉血氧含量下降约30%。9只对照胎儿接受生理盐水。测量平均和搏动性脐血流量、灌注压力、胎盘血管阻力、基础阻抗、压力搏动指数以及校正至胎儿心率160次/分钟的脐动脉阻力指数。在第10天，两组均进行急性栓塞，直至胎儿动脉pH值降至约7.00。使用Sonicaid System 8000（英国牛津牛津Sonicaid公司）测量胎儿心率。
慢性胎儿胎盘栓塞与脐血流量逐渐减少（p < 0.00001）和胎儿动脉血氧含量降低（p < 0.001）相关，而胎儿心率模式保持不变。校正至胎儿心率160次/分钟的脐动脉阻力指数的慢性增加，只有在考虑脐动脉压力搏动指数和基础阻抗的变化以及胎盘血管阻力的变化时才能完全解释。在急性栓塞导致脐血流量减少50%（p < 0.0002）和胎盘血管阻力增加三倍（p < 0.0001）期间，与进行性代谢性酸中毒相关的胎儿心率模式最一致的变化是绝对加速频率降低84%（p < 0.0001），而短期胎儿心率变异性保持不变。
慢性脐-胎盘栓塞导致胎儿低氧血症时，脐动脉阻力指数的变化在胎儿心率模式出现任何可检测变化之前就已发生。绝对加速频率降低是近足月绵羊胎儿与进行性代谢性酸中毒相关的胎儿心率模式的唯一组成部分。
