Shields L E, Brace R A
Department of Reproductive Medicine, University of California, San Diego, La Jolla 92093-0802.
Am J Obstet Gynecol. 1994 Jul;171(1):84-9. doi: 10.1016/s0002-9378(94)70082-6.
This investigation tested the hypothesis that elevations in fetal vascular pressures during nonlabor uterine contractions would be eliminated during polyhydramnios and augmented during oligohydramnios.
Twenty-two chronically catheterized fetal sheep were divided into three groups: (1) control with normal amniotic fluid volume, (2) polyhydramnios produced by amnioinfusion, and (3) oligohydramnios produced by fluid drainage. Fetal arterial pressure, venous pressure, and amniotic fluid pressure were continuously recorded with on-line computer techniques. Amniotic fluid pressure was continuously subtracted from fetal arterial pressure and fetal venous pressure to correct to the fetal zero pressure reference. One minute averages were collected for 30 minutes centered around the nonlabor uterine contraction.
Amniotic fluid pressure increased significantly during nonlabor uterine contractions in the control group. During polyhydramnios the amplitude and duration of the amniotic fluid pressure elevation were similar to those of controls (not significant). During oligohydramnios the duration of the uterine contractions was similar to that of both controls and polyhydramnios groups; however, the amplitude was less (p < 0.001). Fetal vascular pressures increased significantly during nonlabor uterine contractions in the control group (p < 0.001) but did not change significantly during nonlabor contractions in the polyhydramnios group. The contraction-induced elevations in fetal arterial pressure and fetal venous pressure in the oligohydramnios group were significantly greater than those in the control group (p < 0.001).
This study shows that the fetal vascular pressure responses to nonlabor uterine contractions were modified significantly by increases or decreases in amniotic fluid volume. The fact that the fetal arterial pressure and fetal venous pressure responses were augmented during oligohydramnios and eliminated during polyhydramnios suggests that direct compression or a conformational change of the fetus may be the cause of the vascular pressure changes during nonlabor contractions.
本研究检验了以下假设，即羊水过多时非分娩期子宫收缩期间胎儿血管压力升高会消除，而羊水过少时会增强。
22只长期插管的胎羊被分为三组：（1）羊水正常的对照组；（2）通过羊膜腔灌注产生羊水过多的组；（3）通过引流产生羊水过少的组。采用在线计算机技术连续记录胎儿动脉压、静脉压和羊水压力。从胎儿动脉压和胎儿静脉压中持续减去羊水压力，以校正至胎儿零压力参考值。以非分娩期子宫收缩为中心，收集30分钟内的1分钟平均值。
对照组非分娩期子宫收缩期间羊水压力显著升高。羊水过多时，羊水压力升高的幅度和持续时间与对照组相似（无显著差异）。羊水过少时，子宫收缩的持续时间与对照组和羊水过多组相似；然而，幅度较小（p<0.001）。对照组非分娩期子宫收缩期间胎儿血管压力显著升高（p<0.001），但羊水过多组非分娩期收缩期间无显著变化。羊水过少组收缩引起的胎儿动脉压和胎儿静脉压升高显著大于对照组（p<0.001）。
本研究表明，羊水过多或过少会显著改变胎儿血管对非分娩期子宫收缩的压力反应。羊水过少时胎儿动脉压和胎儿静脉压反应增强，羊水过多时则消除，这一事实表明，胎儿的直接受压或构象变化可能是非分娩期收缩期间血管压力变化的原因。
