Amniotic Fluid Pressure Research Articles

Trans membranous fetal movement and pressure sensing

Amniotic fluid surrounds the fetus and acts as an important factor in fetal growth. Abnormally high amniotic fluid volume (polyhydramnios) can alert fetal anomaliesm, and inadequate amount of liquid (oligohydramnios) affects the lung development. Mild polyhydramnios occurs in 17% of pregnancies, whereas oligohydramnios occurs in 4.5% of pregnancies and severe oligohydramnios occurs in 0.7% of all pregnancies out of which, only 16.5% is diagnosed. The fetal mortality rate is high in oligohydramnios. The main objective of this study is to periodically monitor the amniotic fluid in the amniotic sac during the third trimester of pregnancy. The used sensors are fitted in a belt that was strapped around the lower abdomen. The amniotic fluid pressure was sensed using pressure sensor. The fetal movements were measured using an accelerometer.

Hiccups and amniotic fluid regulation in early pregnancy

Hiccups are an unexplained phenomenon and a subject of medical curiosity. They arise through a reflex arc with central control at the level of the medulla, and their primary physiological effect is the generation of negative intra-thoracic pressure. This paper presents the hypothesis that hiccups serve a purpose during the first half of gestation, when they are most prevalent; namely, that they promote amniotic fluid influx to the primitive gut, allowing fluid to be transferred to the foetal and then maternal vasculature. Furthermore, hiccups could be provoked by increasing amniotic fluid volume and pressure, and act in a regulatory capacity. This hypothesis could be tested by studying foetal movements in the first half of gestation, and assessing whether there is correlation with amniotic fluid flux in the developing gut. Ascertaining whether hiccups increase in frequency with increasing amniotic fluid volume would provide evidence for or against a regulatory function.

Treatment of twin–twin transfusion syndrome

Twin–twin transfusion syndrome is characterized by unequal blood exchange from the donor twin to the recipient co-twin through placental vascular anastomoses. Treatment of twin–twin transfusion syndrome consists of serial amnioreduction, septostomy, laser photocoagulation of placental vessels and umbilical cord occlusion of the apparently sick twin. Amnioreduction reduces maternal discomfort due to polyhydramnios and improves fetal circulation by reducing amniotic fluid pressure on the placenta. Septostomy equalizes amniotic fluid pressure between the two gestational sacs. Laser therapy interrupts intertwin blood shunting and restores two independent circulations. Umbilical cord occlusion is offered when signs of imminent death are present, such as hydrops and cardiac failure. Laser therapy is associated with increased neonatal survival rates and lower risk of adverse outcomes compared with other treatments.

A mathematical model of twin-twin transfusion syndrome with pulsatile arterial circulations

The twin-twin transfusion syndrome (TTTS) is a severe complication of monochorionic twin pregnancies caused by a net transfusion of blood from one twin (the donor) to the other (the recipient) through placental anastomoses. To examine the pathophysiology of TTTS evolving through clinical stages I to IV, we extended our mathematical model to include pulsating circulations propagating along the arterial tree as well as placental and cerebral vascular resistances, and arterial wall thickness and stiffness. The model demonstrates that abnormal umbilical arterial flow (TTTS stage III) in the donor twin results from increased placental resistance as well as reduced resistance in the cerebral arteries. In contrast, recipient twin abnormal umbilical arterial flow requires a significantly greater increase in placental resistance, resulting from the compressive effects of high amniotic fluid pressure. Thus simulated abnormalities of donor umbilical arterial pulsations occur in the donor more commonly and earlier than in the recipient. The "normal" staging sequence (I, II, III, IV) correlates with the presence of compensating placental anastomoses, constituting the majority of monochorionic twin placentas. However, TTTS stage III may occur before manifestations of stage II (lack of donor bladder filling), in our model correlating with severe TTTS from a single arteriovenous anastomosis, an infrequent occurring placental angioarchitecture. In conclusion, this mathematical model describes the onset and development of the four stages of TTTS, reproduces a variety of clinical manifestations, and may contribute to identifying the underlying pathophysiology of the staging sequence in TTTS.

Cystic fibrosis transmembrane conductance regulator (CFTR) dependent cytoskeletal tension during lung organogenesis

There is growing evidence for the role of CFTR (cystic fibrosis transmembrane conductance regulator) in lung development and differentiation. The mechanism by which the chloride channel could affect lung organogenesis, however, is unknown. In utero CFTR gene transfer in the fetal lungs of mice, rats, and non-human primates was shown previously to alter lung structure and function. A study of the genes altered in the fetal rat lung following CFTR overexpression was initiated in an effort to determine the molecular mechanism for CFTR-dependent differentiation. In utero gene transfer with recombinant adenoviruses carrying either a reporter gene or CFTR resulted in the increased expression of a number of genes upon microarray analysis. The majority of the genes overexpressed in the CFTR-treated lungs were primarily associated with muscle structure and function. Histological and biochemical characterization of these proteins including myosin heavy chain, heat shock protein 27, and isoforms of myosin light chain showed that CFTR overexpression had a profound effect on smooth muscle contraction-related proteins. The CFTR-dependent regulation of smooth muscle contraction related proteins was shown to be related to chloride and extracellular ATP and was dependent upon the PI3 Kinase and Phospholipase C pathways. The changes in smooth muscle proteins were consistent with CFTR-dependent contractions of the embryonic airway smooth muscle. An assay was developed using fluorescent polystyrene beads to show that CFTR did indeed increase amniotic fluid flow into the fetal lung. Increased amniotic fluid pressure was shown previously to be associated with stretch-induced differentiation of the lung. Evaluation of neonatal respiratory function showed that CFTR-dependent muscle contractions and increased amniotic fluid pressure resulted in accelerated maturation of the neonatal rat lung. In addition, these CFTR-dependent changes were shown to be sufficient to reverse the lung phenotype of the CFTR knockout mouse. Mechanical forces influence lung development through pulmonary distension. CFTR overexpression in the fetal lung altered differentiation and development in the lung. These results are consistent with CFTR influencing lung development by regulating the muscle contractions associated with cytoskeletal tension and stretch induced differentiation. Deficiency of CFTR altering lung development would contribute significantly to the Cystic Fibrosis disease phenotype.

THIS MONTH IN ANESTHESIOLOGY

THIS MONTH IN ANESTHESIOLOGY

Apoptosis and Regression of Embryonic Mesenchyme in the Development of the Middle Ear Spaces

Apoptosis was studied using temporal bones from three fetuses representing different times of gestation and from three neonates. Paraffin-embedded sections 20-μm thick were studied using the terminal deoxynucleotide transferase-mediated dUTP nick-end labeling method based on 3′-end-labeling of fragmented DNA. Phenotyping of the immune cells was performed using regular monoclonal antibodies. In the bone marrow the granulocyte series dominated and the number of cells in the macrophage series was noticeably fewer, with apoptotic cells occurring in both. In the embryonic mesenchyme, solitary apoptotic cells occurred in all locations in both the fetuses and neonates. Apoptosis is a basic factor in the regression of embryonal mesenchyme, but may not be preprogrammed. Basic scientific data obtained from modified tissue cultures show that mechanical forces cause cells to switch between different genetic programs. It is suggested that the act of swallowing causes periodic changes in the amniotic fluid pressure and provides the necessary force for regression of the mesenchyme by apoptosis.

Factors influencing the flow rate through a surgical defect in human fetal membranes.

In order to determine factors influencing the flow rate trough a created defect in human fetal membranes, an ex vivo set-up was used with fetal membranes collected from patients undergoing Caesarean section at term. The membranes were secured at the bottom of a plastic tube and traumatised with needles ranging from 14-26 Gauges (Ga), under a hydrostatic pressure of 10 to 20 cm H(2)O and an angle of 45 degrees or 90 degrees. The column was filled with amniotic fluid or Hartmann's solution. The duration of the puncture was 1 s or the time it takes to aspirate 10 ml through the needle. The flow rate through the defect in the fetal membranes and size of the defect were measured. The flow rate and defect size increased with increasing diameter of the needle. Increasing the pressure in the column resulted in a significant linear increase in the flow rate. Replacing the saline solution with amniotic fluid did not result in significant changes in the measured flow rates, except for the small needle size (24 Ga). Increasing the duration of the puncture did not result in increased flow rates, except for small needle size (24 Ga). These experiments suggest that needle diameter, angle of needle insertion, duration of the procedure, amniotic fluid pressure and composition could influence the incidence of amniotic fluid leakage following amniocentesis.

Fetal urine and amniotic fluid in monochorionic twins with twin-twin transfusion syndrome: Simulations of therapy

Objective: Therapy for twin-twin transfusion syndrome includes amnioreduction, septostomy, and laser ablation, but there is no accepted standard of care. Mechanisms for the reported improvement in survival are incompletely understood. We sought to model the mechanisms and predict the response of varying severities of twin-twin transfusion syndrome and placental angioarchitectures to current therapies to determine optimal clinical interventions. Study Design: We used our mathematic model of twin-twin transfusion syndrome that predicts fetal and amniotic fluid abnormalities that are related to the placental angioarchitecture. Amnioreduction was modeled as reduction in amniotic fluid volume; septostomy was modeled as the merging of donor and recipient amniotic fluid, and laser ablation was modeled as the cessation of all placental anastomotic blood flows. Results: Amnioreduction reduces amniotic fluid pressure, which improves transplacental fluid flow from mother to fetus and increases both donor and recipient blood volume. However, net arteriovenous transfusion increases, because of increased donor arterial pressure, which negates, in part, the benefit of amnioreduction. Septostomy allows amniotic fluid to be swallowed by the donor, with minimal effects on donor growth and blood volume. Laser ablation eliminates anastomotic exchange of blood and reduces discordant fetal growth. Conclusion: Amnioreduction may be effective in milder twin-twin transfusion syndrome pregnancies but ineffective in severe cases. Septostomy is unlikely to offer significant therapeutic efficacy. Laser ablation is equally effective in mild and severe twin-twin transfusion syndrome but has a higher spontaneous abortion rate than amnioreduction. The model indicates improved outcomes with the use of amnioreduction in mild twin-twin transfusion syndrome cases and with laser ablation in severe cases. (Am J Obstet Gynecol 2001;185:996-1003.)

Polyhydramnios and arterio-arterial placental anastomoses maybeneficially affect monochorionic twin pregnancies

Our objective was to appraise whether an increased amniotic fluid pressure bypolyhydramnios can beneficially affect monochorionic twins that arehaemodynamically connected by arterio-venous plus arterio-arterial placentalanastomoses. We assessed the effects of polyhydramnios in monochorionic twinplacentas, combining (a) data from previous in vitro placentalperfusion experiments in singleton term placentas under simulated normal andincreased amniotic fluid pressures with (b) logical deduction fromobservations made in monochorionic twins. Our hypothesis is that inmonochorionic placentas, an increased amniotic fluid pressure increases theplacental microvascular resistance but not the resistance of placentalchorionic plate arteries. Hence, an increased amniotic fluid pressureincreases the microvascular resistance of the joint cotyledon, thearterio-venous resistance, but not the arterio-arterial resistance. Thisproposed mechanism reduces arterio-venous but not oppositely directedarterio-arterial transfusion. Therefore, reversal of the normal direction ofnet foeto-foetal transfusion may develop, which will reduce the circulatoryimbalance that evolved between the monochorionic foetal twins. In contrast, inmonochorionic twins connected by unidirectional or bidirectionalarterio-venous anastomoses reversal of the normal direction of net foeto-foetaltransfusion will not occur. In conclusion, reversal of the normal direction ofnet foeto-foetal transfusion, induced by polyhydramnios, is protective againstthe onset and severity of twin-twin transfusion syndrome in monochorionictwins connected by arterio-venous plus arterio-arterial anastomoses, but notby unidirectional or bidirectional arterio-venous anastomoses.

Amniotic Fluid Pressure in Both Cavities of Twin-to-Twin Transfusion Syndrome: A Vote against Septostomy

Objective: To report our results of the measurement of the amniotic fluid pressure in twin-to-twin transfusion syndrome before and after amniodrainage and the separate measurement in the cavity of the stuck twin and the recipient, respectively, in 2 cases. Method: Six patients with severe TTS underwent therapeutic amniodrainage. Amniotic fluid pressure was obtained before and after reduction of the fluid volume. In 2 of these cases we were able to calculate the pressure separately in both amniotic cavities, the donors (stuck twin) and the recipients. Results: In all cases of TTS, amniotic pressure was high before and reduced after amniodrainage. The pressure was equal in the donors and in the recipients cavity. Conclusion: Amniotic pressure seems to be high in TTS, but equal in both cavities. Therefore, amniotic septostomy is probably of low value, especially if a high-risk monoamniotic situation is artificially created.

Effect of high amniotic fluid pressure on fetal circulation.

The purpose of this study was to investigate the effects of high amniotic fluid pressure (AFP) created by amnioinfusion on fetal circulation. Five pregnant goats whose fetuses had a mean gestational age of 131 +/- 2 days (term 145 days) were used. After a 30 minute control period, 1500 ml of warm saline was infused to the amniotic cavity over a period of 30 minutes. The AFP gradually increased during amnioinfusion and remained 2-3 mmHg above the control level for 3 hours after amnioinfusion. Fetal arterial pH (FpH) tended to decrease, and there was a significant negative correlation between the FpH and AFP (r = -0.723). Fetal arterial pO2 also tended to decrease and negatively correlated to the AFP (r = -0.59). On the other hand, fetal arterial pCO2 tended to increase and positively correlated with the AFP (r = 0.75). Although amnioinfusion is useful for improving the status of a distressed fetus, the fetal condition may be jeopardized at the same time. Therefore, careful monitoring of the AFP and fetal status is recommended during amnioinfusion.

Equalization of Amniotic Fluid Volumes after Decompression Amniocentesis for Treatment of the Twin Oligohydramnios-Polyhydramnios Sequence

Objective: To measure acute and chronic changes in the placenta and amniotic fluid associated with performance of decompression amniocentesis in pregnancies with the twin oligohydramnios-polyhydramnios sequence (TOPS). Methods: Amniotic fluid pressures, placental thickness, placental perfusion, and amniotic fluid volumes were measured in each sac of a monochorionic diamniotic twin gestation before and after decompression amniocentesis. Indigo carmine was injected into the polyhydramnic sac after decompression, and fluid from the oligohydramnic sac was sampled after equilibration. Spectrophotometric analysis of amniotic fluid specimens was performed for dye detection. Amniotic fluid volume and placental perfusion studies were repeated 1 week later. Results: Three patients with TOPS were enrolled, and decompression amniocentesis was performed in the midtrimester. After decompression, amniotic fluid volume decreased in the polyhydramnic sac, amniotic fluid pressures decreased in both sacs, placental thickness increased, and umbilical artery Doppler velocimetry was unaffected. The amniotic fluid volume increased acutely in only one oligohydramnic sac after decompression, and ultrasonographic examination, amniotic fluid spectrophotometric analysis, and placental pathologic examination all identified interfetal membrane disruption as the etiology. Conclusions: Decompression amniocentesis as a treatment for TOPS does not result in acute or chronic changes in the amniotic fluid volume of the oligohydramnic sac in the absence of interfetal membrane disruption.

Chorionic plate vascular anatomy determines the efficacy of amnioreduction therapy for twin-twin transfusion syndrome.

The objective of the study was to determine whether vascular anatomy of monochorial placenta influences the therapeutic efficacy of serial amnioreduction in chronic mid-trimester twin-twin transfusion syndrome (TTTS). Twenty-six consecutive monochorial pregnancies complicated by TTTS and treated by serial amnioreduction were studied. The placental anastomoses were delineated postnatally by perfusion studies. Amniotic fluid index, amniotic fluid pressure, number of amnioreductions, interval between amnioreduction, and neonatal outcome were correlated with the presence or absence of superficial anastomotic channels and type of cord insertion. Placentae were divided into two groups according to the presence (n = 9) and absence (n = 14) of superficial anastomosis. Gestational age at diagnosis, delivery, percentage discordance in estimated birth weight were comparable in the two groups. The amniotic fluid index, liquor volume removed, and amniotic pressure at first amnioreduction were also comparable between groups. In the group without superficial arterio-arterial/veno-venous (AA/VV) anastomoses, amnioreduction was required more often (P < 0.05). Perinatal mortality in terms of intrauterine deaths (IUD) and neonatal death was more common in the group without AA/VV anastomotic channels (P < 0.05). There was no difference in incidence of velamentous/marginal cord insertion between the two groups. TTTS lacking superficial AA or VV anastomosis are more likely to require frequent amnioreduction and are associated with increased perinatal mortality and morbidity, whereas the presence of such shunts was associated with increased therapeutic efficacy of amnioreduction and a more favourable prognosis.

Effects of intravascular transfusion for red cell alloimmunization on fetal arterial blood pressure.

To evaluate the effects of intravascular transfusion (IVT) on the fetal umbilical arterial pressure (UAP) in pregnancies complicated by red cell alloimmunization. UAP and amniotic fluid pressures (AFP) were measured immediately before and after IVT. Mean UAP was calculated by computing 1/3 (systolic blood pressure - diastolic blood pressure) + diastolic blood pressure. The fractional increase in fetoplacental blood volume with transfusion was calculated by dividing the net volume of blood transfused by the sum of the net volume transfused and the fetoplacental volume based on the estimated fetal weight by ultrasound. Statistical techniques included paired t-test, and the Pearson product correlation. Significance was defined as p < 0.05. The fetal umbilical artery was punctured during a total of 27 procedures in 21 patients. Pre- and posttransfusion mean UAPs were recorded in 16 of these procedures. Mean UAP increased from 34.0 +/- 14.2 mm Hg pretransfusion to 38.6 +/- 12.8 mm Hg posttransfusion (p = 0.34). There was no correlation between the fractional change in fetoplacental blood volume and the calculated difference between pre- and posttransfusion blood pressure. Bradycardia occurred during 5 procedures (31.2%). Fetal demise occurred after 2 procedures (12.5%). IVT appears to have a minimal effect on the fetal UAP. Fetal bradycardia occurs in a significant percentage of these cases.

Umbilical venous pressure is unaltered by severe, early-onset growth restriction.

To determine whether severe, early-onset intrauterine growth restriction (IUGR) is associated with abnormal umbilical venous pressure (UVP) secondary to increased placental impedance. 42 singleton fetuses underwent fetal blood sampling from the umbilical vein during evaluation for severe, early-onset IUGR (diagnosed < 32 weeks or symmetrical IUGR diagnosed at any time in gestation). IUGR was confirmed at delivery. The UVP was measured with a solid-state transducer and corrected for amniotic fluid pressure. The ultimate cause of IUGR assigned was based on the antenatal laboratory and postnatal findings. Seven fetuses had a chromosome abnormality, 4 congenital viral infection, 8 miscellaneous causes and 23, by exclusion, uteroplacental (UP) dysfunction. Procedures complicated by fetal bradycardia were excluded because bradycardia raises the UVP. The mean gestation was 31.4 weeks (range 23-38). The umbilical artery resistance index (UA RI) was significantly higher in fetuses with IUGR secondary to either UP dysfunction or a chromosome abnormality compared to the remaining categories of IUGR. The UVP fell outside the 95% confidence interval in only 3 fetuses - 2 with aneuploidy (a 1:7 translocation with a normal UA RI and a mosaic trisomy 21), and 1 with UP dysfunction. The UVP rose with advancing gestation independent of the underlying cause of IUGR. There was an inverse relationship between UVP and the UA RI independent of gestation (r2 = 0.08, p < 0.05). There was an inverse relationship between the UA RI and both the UV pH and PO2 in the fetuses with UP dysfunction. However, there was no relationship between the UVP and either UVpH, UVPCO2, or UVpO2. These findings indicate that placental impedance has little clinically relevant impact on the UVP.

Amniotic fluid pressure in twin-to-twin transfusion syndrome: an objective prognostic factor.

Severe twin-to-twin transfusion syndrome presenting before 28 weeks' gestation is associated with a high neonatal mortality and morbidity due to polyhydramnios-related very premature delivery or intrauterine death of one or both twins. Management options include serial amniodrainages or laser coagulation of the intertwin placental anastomoses; however, early antenatal prognostic factors are lacking. Serial amniocenteses were performed in 9 pregnancies with twin-to-twin transfusion syndrome presenting with second-trimester polyhydramnios, and serial measurements of amniotic fluid pressure were made. Although in 8 cases the pre-drainage pressure was above the 95th centile of the normal range for singleton pregnancies, the pressures were lower in the pregnancies resulting in two livebirths than in the cases where one or both babies died. This study suggests that patients presenting with intraamniotic pressure > 17 mm Hg cannot be safely managed by serial amniodrainages.

Reversible tracheal obstruction in the fetal sheep: Effects on tracheal fluid pressure and lung growth

Congenital diaphragmatic hernia (CDH) continues to carry high morbidity and mortality. A number of treatment modalities including extracorporeal membrane oxygenation and in utero repair have improved the mortality rate only minimally. With this condition, there is often insufficient lung mass at birth and persistent pulmonary hypertension postnatally. Experimental fetal tracheal ligation has been shown to increase lung growth in utero and to reduce the hernial contents in CDH. The purpose of this study was to determine the effect of reversible fetal tracheal occlusion on tracheal pressure and lung development. Nine fetal sheep were divided into two groups. Group 1 had intratracheal balloons placed, and the balloons were left inflated for 21 to 28 days. Group 2 consisted of littermates that served as controls. They either had uninflated balloons placed or were left unoperated. Tracheal pressure measurements were recorded periodically, and the amniotic fluid pressure served as a reference. The animals were killed near term, and the lungs, heart, and liver were weighed and corrected for body weight. Standard morphometry was used to compare the lungs further, and the lung DNA and protein content were measured. Tracheal damage from the balloon catheter also was assessed. The tracheal pressure was 3.85 (±.49 SE) mm Hg in experimental animals, and it averaged −0.27 (±.27 SE) mm Hg in controls ( P < .0001). Tracheal occlusion increased lung weight and volume by two to three times ( P < .0001 and P < .0006, respectively) while heart and liver weights remained similar to those of controls. The airspace fraction and radial alveolar counts were increased ( P = .044 and P = .0002, respectively), and the alveolar number per body weight was doubled ( P < .0001). However, the alveolar number per lung volume was preserved, as were the DNA and protein content per unit weight of lung tissue. The chronic indwelling balloon catheter caused some mucosal and submucosal damage at the balloon site and proximal to it. These results show that tracheal occlusion leads to an elevation of intratracheal pressure that is associated with a tremendous increase in lung growth over a short period in third-trimester fetal sheep. The techniques used in this experiment can be easily modified for use with endoscopic surgical equipment.

Potential route for fetal therapy: Intramembranous absorption of intraamniotically injected furosemide

OBJECTIVE: Our purpose was to determine whether intraamniotically injected furosemide could be absorbed directly into fetal circulation by the ovine intramembranous pathway. STUDY DESIGN: Nine chronically catheterized fetal sheep, five with an intact and four with a surgically ligated esophagus, were studied for 7 hours on 2 consecutive days. Day 1 was a control day in which the fetal parameters of arterial, venous, and amniotic fluid pressures; heart rate; and urine flow were measured continuously. Fetal and maternal blood, amniotic fluid, and fetal urine were sampled for osmolality, electrolytes, blood gases, and pH twice during the first hour and hourly thereafter. On day 2, 15 mg of furosemide was injected into the amniotic cavity after 1 hour and fetuses were monitored in the same fashion as on the control day. RESULTS: On day 2, both intact and ligated fetuses demonstrated a rapid and prolonged increase in urine flow ( p < 0.01) compared with control day fetuses. Esophageal ligation decreased, but did not eliminate, he diuresis. Free water clearance increased equally ( p < 0.05) in both groups compared with control fetuses. Sodium and chloride excretion increased significantly in intact (sodium 591% ± 220% and chloride 763% ± 295%) and ligated fetuses (sodium 234% ± 70% and chloride 409% ± 74%) compared with control fetuses. CONCLUSIONS: Diuresis after esophageal ligation demonstrates that furosemide is absorbed by the ovine intramembranous pathway.

Fetal vascular pressure responses to nonlabor uterine contractions: Dependence on amniotic fluid volume in the ovine fetus

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.