Effects of maternal oxygen administration on fetal oxygenation during reductions in umbilical blood flow in fetal lambs

In 11 chronically catheterized fetal lambs (123 +/- 6, mean +/- SD, days of gestation; term = 147 days), we measured fetal oxygen delivery and oxygen consumption before and during reductions in umbilical blood flow (Qumb). Qumb was reduced by inflation of a balloon occluder located just proximal to the origin of the common umbilical artery. Measurements were made while the unanesthetized maternal sheep received either room air or 100% oxygen to breathe. In oxygen-treated fetuses, oxygen concentrations in umbilical venous blood (Cuvo2) and arterial blood (Cao2) were increased over a wide range of Qumb when compared with those of room air-treated fetuses. Because of these responses, fetal oxygen delivery (Do2 = Qumb X Cuvo2) and oxygen consumption [Vo2 = Qumb(Cuvo2-Cao2)] were greater in oxygen-treated fetuses than in room air-treated fetuses during episodes of reduced Qumb. In oxygen-treated fetuses, Vo2 decreased from normal levels only when Qumb was less than or equal to 75 ml/min/kg of fetus, whereas in room air-treated fetuses Vo2 decreased at Qumb less than or equal to 150 ml/min/kg. Our data indicate that oxygen administration to the pregnant sheep increases oxygen delivery to the fetus during times of reduced umbilical perfusion and that this supplemental oxygen supply provides an oxygen reserve with which the fetus can maintain oxidative metabolism. These data may be relevant to those clinical conditions, such as umbilical cord compression in labor, that are associated with reductions in umbilical blood flow.     

The influence of beta-adrenergic activity on fetal heart rate and the umbilical circulation during hypoxia in fetal sheep

To determine the importance of beta-adrenergic activity during hypoxia in the fetus, 13 studies were carried out on seven chronically instrumented sheep at nine tenths of gestation. Hypoxia was induced by having the mother breathe gas mixtures that resulted in a reduction of maternal arterial oxygen tension to 32 mm Hg. Hypoxia resulted in a decrease in fetal heart rate (165 +/- 17 to 140 +/- 28 bpm) and fetal oxygen consumption (5.9 +/- 1.3 to 3.0 +/- 1.5 ml/min/kg) and increases in fetal arterial and umbilical venous pressures. There was no change in umbilical blood flow (209 +/- 58 ml/min/kg). Propranolol, 1.1 ml/kg, was rapidly infused into a fetal vein to achieve complete beta-adrenergic blockade. Umbilical vascular resistance increased significantly, fetal heart rate decreased to 112 +/- 22 bpm, and umbilical blood flow decreased to 165 +/- 73 ml/min/kg. There was no further decrease in fetal oxygen consumption. These decreases are approximately twice those seen after propranolol without hypoxia. These findings suggest that during hypoxia there is an increase in beta-adrenergic activity, which tends to maintain fetal heart rate and umbilical blood flow. This activity counteracts the increase in vagal activity with hypoxia, which decreases heart rate.     

Effects of maternal anemia on uteroplacental and fetal oxidative metabolism in sheep

We studied the effects of acute isovolemic maternal anemia on several variables of uterine and fetal oxygenation to answer these two questions: (1) Does maternal anemia cause reductions in oxygen delivery to the uterus, placenta, and fetus? (2) If so, what is the impact of such reductions on fetal oxidative metabolism? In 15 chronically catheterized pregnant sheep and fetal lambs, we measured uterine and umbilical blood flows and uterine and fetal oxygen deliveries, oxygen extractions, and oxygen consumptions at various, randomly selected maternal hematocrits ranging from 30% to 8%. We altered maternal hematocrit by performing isovolemic exchange transfusions with plasma or packed red blood cells. Uterine and umbilical blood flows were measured with the radionuclide-labeled microsphere technique, and the variables of oxygenation were calculated with modifications of the Fick principle. Decreases in maternal hematocrit led to linear reductions in oxygen delivery to the uterus, placenta, and fetus. Despite reductions in oxygen delivery of up to 50%, fetal oxygen consumption was maintained, because of compensatory increases in oxygen extraction. When hematocrit (and thus fetal oxygen delivery) was reduced by more than 50%, fetal oxygen consumption and the arterial blood base excess both decreased, indicating that, at these hematocrit levels, the supply of oxygen to fetal tissues was inadequate for the demands for oxygen by these tissues.     

Single dose of labetalol in hypertensive pregnancy: effects on maternal hemodynamics and uterine and fetal flow velocity waveforms.

The short-term effect of 0.8 mg/kg of an intravenous bolus of labetalol on maternal and fetal hemodynamics was investigated in ten women with pregnancy-induced hypertension. The maximum effect occurred within 35 minutes after labetalol administration. At that point, the mean arterial pressure had decreased by 18% and there was a slight decrease in maternal heart rate. As to flow velocity waveforms, no significant change was found in mean systolic/diastolic (S/D) ratio of the uterine artery, umbilical artery or fetal middle cerebral artery. However, in two subjects with a marked reduction in blood pressure also the uterine artery S/D ratio decreased.     

Umbilical artery pulsatility index and placental vascular resistance during acute hypoxemia in fetal lambs

The effect of hypoxemia on the pulsatility index (PI) of the umbilical artery flow velocity waveform and placental vascular resistance was studied. Fetal hypoxemia was induced by maternal breathing of a low-oxygen gas mixture. Umbilical venous blood flow was measured with an electromagnetic flowmeter. Placental vascular resistance (PVR) was defined as the ratio perfusion pressure (mean arterial pressure minus umbilical venous pressure) and umbilical blood flow. Umbilical artery velocity waveforms were obtained by a 5-MHz pulsed Doppler device around one umbilical artery in 4 lambs and by a transcutaneous 4-MHz continuous wave Doppler transducer in 3 lambs. Fetal arterial oxygen content was lowered from 2.28 +/- 0.18 to 0.93 +/- 0.15 mM (p less than 0.05), while pCO2 and pH remained unchanged. Control values of the hemodynamic variables were compared with values during deepest hypoxemia. Fetal heart rate, mean arterial and umbilical venous pressure, PVR and the umbilical artery PI did not significantly change, whereas umbilical blood flow increased from 436 +/- 64.7 to 491 +/- 65.9 ml/min (p less than 0.05) during deepest hypoxemia. Individual regression analysis, however, showed a significant inverse correlation of umbilical venous pressure whereas PVR had a positive correlation with actual oxygen content. It is concluded that acute fetal hypoxemia slightly decreases PVR, but does not affect the umbilical artery PI in sheep. Decreasing fetal oxygenation is associated with an increase in pressure in the umbilical vein.     

Oxytocin in maternal and fetal blood.

Radioimmunoassayable plasma oxytocin (OT) has been measured in maternal and fetal blood. Simultaneous samples were obtained in maternal forearm venous blood and in umbilical venous and arterial blood in 29 patients at term delivery. In addition, maternal forearm venous blood samples were also obtained 10 minutes prior to delivery. Mean OT level in maternal plasma at delivery was 82 +/- 12 muU/ml, and at 10 minutes prior to delivery the mean OT level was 90 +/- 11 muU/ml. The umbilical arterial plasma OT showed 95 +/- 12 muU/ml and the umbilical vein plasma OT was 60 +/- 10 muU/ml. Oxytocin levels higher in maternal blood than in fetal blood were found with the following incidence: In 51% of samples there was more OT in maternal venous blood than in umbilical arterial blood, and in 84% of samples there was more OT in maternal blood than umbilical vein blood. During the postpartum period, the mean maternal plasma OT was 66 +/- 8 muU/ml for the first day, and 50 +/- 9 muU/ml and 54 +/- 9 muU/ml for the second and third days, respectively. This study indicates that both the fetus and the mother are active producers of oxytocin.     

The effect of insulin on ovine fetal oxygen extraction

Infusion of exogenous insulin (54 +/- 19 mU/kg/hr) to seven fetal lambs caused hyperinsulinism and arterial hypoxemia but not hypoglycemia. We measured the relationship between fetal oxygen delivery and oxygen use for a better understanding of the cause of the observed hypoxemia. Oxygen delivered to the fetus is the product of fetal umbilical venous oxygen content and umbilical blood flow. Both of these quantities decreased as fetal insulin concentration rose. The fall in umbilical blood flow was due to a change in the distribution of cardiac output. Cardiac output rose, but placental perfusion decreased while blood flow to the fetal carcass increased. Oxygen consumption by the ovine fetus increased as insulin concentration rose. Since the delivery of oxygen to the fetus did not increase when its use was rising, fetal extraction of available oxygen increased. Fetal arterial hypoxemia is the result of this increased extraction of available oxygen.     

The effect of acute maternal hypoxia on fetal oxygenation and the umbilical circulation in the sheep

The mean oxygen consumption was 8.4 ± 1.9 ml/min/kg in the near-term fetal sheep. In response to acute maternal hypoxia fetal O₂ consumption decreased to lower than 50% of the control values. The decrease was rapidly instituted, proportional to the degree of hypoxia, sustained for up to 47 min and stable over this period. With increasing duration of hypoxia, a progressive metabolic acidosis developed. Recovery of oxygen consumption occurred rapidly after hypoxia ceased, though the acidosis was not resolved until 2 h later. Umbilical blood flow was maintained during maternal hypoxia and umbilical arterial and venous pressures increased. A fetal bradycardia invariably accompanied the hypoxia.     

The effect of maternal oxygen administration on fetal and maternal blood flow values using Doppler ultrasonography.

Thirty-one pregnant women divided into three groups (AGA prepartum, SGA prepartum without distress, AGA in labor) were examined using Doppler ultrasonography before, during and after oxygen administration to mothers via a face mask. The aim of the study was to find out if there was any effect on the blood flow values in the fetal aorta, the umbilical artery, the fetal common carotid artery and the uterine arcuate arteries. The resistance index (RI) did not change in those vessels during maternal hyperoxygenation with one exception: in the group of SGA fetuses the RI in the fetal aorta increased significantly. Blood flow velocity and volume blood flow remained unchanged in the fetal aorta during oxygen administration.     

Effect of Ro 61-1790, a selective endothelin-A receptor antagonist, on systemic and uterine hemodynamics and fetal oxygenation in sheep.

OBJECTIVE: Endothelin-1 is reportedly elevated in preeclampsia, and studies in our laboratory have shown that infusion of endothelin-1 produces increased mean arterial pressure, hemoconcentration, and proteinuria, while decreasing uterine blood flow. If a role in preeclampsia is confirmed for endothelin-1, therapeutic intervention may involve selective endothelin-A receptor blockers. Thus, this study was designed to determine the effects of Ro 61-1790, a selective endothelin-A receptor inhibitor, on mean arterial pressure, heart rate, and uteroplacental blood flow in pregnant and nonpregnant sheep. STUDY DESIGN: Seven pregnant and seven nonpregnant sheep were instrumented with indwelling femoral artery and vein catheters and bilateral uterine artery flow probes, allowing determination of mean arterial pressure, heart rate, and uteroplacental blood flow. After baseline administration, animals received intravenous Ro 61-1790 either 1 mg/kg or 3 mg/kg, and hemodynamic responses were monitored for 120 minutes. RESULTS: Intravenous administration of Ro 61-1790 at 1 mg/kg had no effect on the parameters measured in either group studied. However, at 3 mg/kg, Ro 61-1790 caused an increase in total uterine blood flow in nonpregnant sheep from 22 +/- 6 mL/min to 51 +/- 15 mL/min. This occurred in the absence of significant changes in mean arterial pressure. In pregnant animals, administration of 3 mg/kg Ro 61-1790 decreased mean (+/- SEM) uteroplacental blood flow by 20% (from 771 +/- 130 mL/min to 621 +/- 110 mL/min) and increased uterine vascular resistance transiently. Administration of Ro 61-1790 had no significant effect on fetal mean arterial pressure, heart rate, or oxygenation. CONCLUSIONS: These data suggest that endogenous endothelin-1 may play an important role in regulating uterine vascular tone in pregnant and nonpregnant sheep and that inhibition of endogenous endothelin-1 may lead to reductions in uteroplacental perfusion in pregnant animals.     

Effects of maternal exercise using bicycle ergometer on maternal heart rate, blood pressure, oxygen consumption and fetal heart rate

The effects of maternal exercise on pregnant women and fetal well-being are largely unknown. Forty-eight pregnant women between 16 and 39 weeks' gestation were exercised on a bicycle ergometer. We studied the oxygen consumption, blood pressure, maternal and fetal heart rate (FHR) at rest, during and after the exercise. The mean maternal heart rate and blood pressure were increased to 166.1 +/- 12.2/min (mean +/- S.D., n = 48) and 161.1 +/- 20.1/82.7 +/- 15.2 mmHg, respectively, at maximal exercise. The absolute oxygen consumption (1/min) was increased with advancing pregnancy at rest and maximal exercise, but the functional oxygen consumption (ml/kg/min) was not changed during pregnancy. The mean FHR was increased about 4 and 9 bpm in the 2nd and 3rd trimesters, respectively. Abnormal FHR patterns after the exercise were observed in 8 cases (16.7%), mild tachycardia: 6 cases, deceleration: 2 cases. Increasing the maternal heart rate at maximal exercise, increased the frequency of the abnormal FHR pattern. When the maternal heart rate was below 160/min, there was no abnormal FHR pattern. These results suggest that several medical checks should be done not only for the mother but also for her fetus during exercise and the maternal heart rate should not exceed 160/min.     

Uterine vascular resistance during compression of the umbilical arterial and/or venous circulation in sheep

Total umbilical cord occlusion and selective occlusion of the umbilical arteries and veins is associated with changes in uterine blood flow. In the present study, the resistance to uterine blood flow during selective occlusions of the umbilical arteries and/or veins was analysed in five chronically instrumented pregnant sheep in the last third part of pregnancy. An occluding device which allows separate occlusion of umbilical veins and arteries was applied to the umbilical cord. Median uterine artery blood flow was measured using an electromagnetic flow meter. Maternal pressures were measured in a branch of the uterine artery and vein. Two occlusions of the umbilical veins and/or arteries with a duration of 30-60 s were performed in each animal. Selective occlusion of the umbilical arteries resulted in a small increase in uterine blood flow from 637 +/- 79 ml/min during control toward 664 +/- 77 ml/min at the end of occlusion (p less than 0.05). Uterine perfusion pressure (uterine arterial pressure - uterine venous pressure) did not change. No changes were observed in calculated uterine vascular resistance (Poiseuille equation). Selective occlusion of the umbilical veins on the other hand caused a decrease in uterine blood flow from 617 +/- 75 ml/min during control to 546 +/- 69 ml/min at the end of occlusion (p less than 0.001), and a return to control value at 1 min after occlusion. The uterine perfusion pressure increased from 40.1 +/- 6.8 mmHg during control to 42.8 +/- 7.0 mmHg at the end of occlusion (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Ten-minute umbilical cord occlusion markedly reduces cerebral blood flow and heat production in fetal sheep

OBJECTIVE: The study was undertaken to determine to what extent a 10-minute total umbilical cord occlusion affects autoregulation of cerebral blood flow and cerebral heat production in the fetus. STUDY DESIGN: In seven chronically catheterized late-gestation fetal sheep (127-131 days' gestation), we studied fetal blood gas, hemodynamic, and thermal responses to 10-minute total umbilical cord occlusion. RESULTS: Ten-minute umbilical cord occlusion resulted in marked hypoxia/ischemia, with oxygen content decreasing from 6.5 +/- 0.4 to 0.6 +/- 0.1 vol% and lactate concentration increasing from 1.8 +/- 0.2 to 10.7 +/- 0.7 mmol/L. During this period, the fetuses showed reductions in heart rate from 163.5 +/- 3.4 to 97.1 +/- 5.4 beats/min, mean arterial pressure from 39.4 +/- 2.1 to 21.2 +/- 2.5 mm Hg, cerebral blood flow from 101.3% +/- 8.9% to 49.7% +/- 10.3%, and cerebral heat production from 95.0% +/- 6.3% to 29.6% +/- 4.8%. During cord occlusion, cerebral blood flow was pressure passive from the fourth minute onward. The reduction in cerebral heat production preceded the reduction in perfusion pressure and cerebral blood flow. Recovery of cerebral blood flow and heat production to control values was incomplete for more than 60 minutes after restoration of umbilical flow. CONCLUSION: Ten-minute total umbilical cord occlusion results in major reductions in cerebral blood flow and heat production. Autoregulation of cerebral blood flow was lost within 4 minutes of occlusion, probably as a result of hypoxia, combined with hypotension. The fact that the reduction in cerebral heat production preceded and exceeded the reduction in blood flow may suggest active down-regulation of cerebral metabolism, the mechanism of which is unclear at present.     

Blood flow velocity in the fetal abdominal aorta and in the umbilical artery in uncomplicated pregnancies.

The blood flow velocity waveform (BFWV) in fetal vessels depends on the stroke volume and the frequency of the fetal heart, the compliance of the vessel and the peripheral resistance of the fetal vascular bed. The objective of the present study was to establish the change of the BFVW throughout gestation and whether the change of the resistance indices are related to the peak flow velocity and/or the end-diastolic flow velocity. The BFVW of the fetal abdominal aorta and of the umbilical artery at 27th-30th week and at 37th-40th week of gestation were analysed in fifteen patients with uncomplicated pregnancies and subsequent normal outcome. The measurement was performed with a pulsed duplex scanner (Kranzbühler). The Doppler beam had a fixed angle of 50 degrees to the fetal vessel in all cases. The peak flow velocity in the fetal aorta remained constant from the 27th-30th week to the 37th-40th week of gestation: 1418 +/- 248 Hz vs. 1448 +/- 269 Hz. The end-diastolic flow, however, showed a significant increase during the respective periods: from 270 +/- 59 Hz to 325 +/- 69 Hz. The peak flow velocity in the umbilical artery was about 25% below that of the fetal aorta: 1028 +/- 149 Hz (27th-30th week) and 1106 +/- 196 Hz (37th-40th week). The end-diastolic flow, however, increased by about 41%: 292 +/- 86 Hz vs. 412 +/- 83 Hz demonstrating a tremendous change of the compliance and the peripheral resistance in the umbilical vascular system. These alterations are also exhibited by the resistance indices. The resistance indices S/D, PI and RI of both vessels were related to the EDF of the abdominal aorta and the umbilical artery at the respective gestational age. It demonstrated that the EDF is of major influence on the calculated resistance indices. The blood flow in the aorta and the umbilical artery was 135(+/- 18) ml/kg/min and 143 (+/- 21) ml/kg/min, respectively. In conclusion, the BFVW for fetal surveillance should be measured under a constant angle in the fetal abdominal aorta. It gives a good information concerning the peripheral resistance and compliance in the respective vascular areas. The EDFV has its lowest value at 200 Hz in the fetal aorta and in the umbilical artery under physiological conditions.     

Circulatory responses to prolonged hypoxemia in fetal sheep

Experiments were conducted in 11 chronically catheterized pregnant sheep to determine the distribution of blood flow within the fetus during prolonged (48 hours) hypoxemia secondary to the restriction of uterine blood flow. Uterine blood flow was mechanically restricted with a polytetrafluoroethylene vascular clamp placed around the maternal common internal iliac artery such that mean (+/- SEM) fetal arterial oxygen tension decreased from 23.4 +/- 1.9 to 17.3 +/- 0.8 mm Hg at 1 hour of hypoxemia and remained low for 48 hours. There was an initial increase in fetal arterial carbon dioxide pressure from 48.5 +/- 0.9 mm Hg during the control period to 56.2 +/- 2.3 mm Hg at 1 hour; this parameter subsequently returned to control values, whereas base excess showed a transient decrease. Fetal cerebral, myocardial, and adrenal blood flows were significantly increased at 1, 24, and 48 hours of hypoxemia. In contrast, there was no change in nuchal muscle or renal blood flows with hypoxemia of this magnitude. Cotyledonary blood flow increased transiently by 38% at 1 hour of hypoxemia, but was not changed from control at 24 and 48 hours. These experiments demonstrate that the sheep fetus is able to maintain the normal protective circulatory adjustments seen with acute hypoxemia for up to 48 hours in the absence of progressive metabolic acidemia.     

Role of prostaglandins in the metabolic responses of the fetus to hypoxia.

OBJECTIVE: The effect of inhibiting prostaglandin synthesis on the fetal metabolic response to hypoxemia was examined by infusing indomethacin during periods of reduced maternal uterine blood flow. STUDY DESIGN: In seven fetal sheep we administered a 6-hour infusion of either indomethacin (n = 5), indomethacin plus prostaglandin E2, or a vehicle solution (n = 5). The last 4 hours of each infusion period coincided with a period of fetal hypoxemia induced by reduced maternal uterine blood flow. RESULTS: During reduced maternal uterine blood flow indomethacin infusions caused a significantly greater reduction in pHA (reduced from 7.36 +/- 0.01 to 7.10 +/- 0.02) than both the vehicle (from 7.36 +/- 0.01 to 7.20 +/- 0.03) and indomethacin plus prostaglandin E2 infusions (from 7.36 +/- 0.01 to 7.18 +/- 0.02). Before reduced maternal uterine blood flow was induced, indomethacin significantly elevated fetal plasma glucose and lactate concentrations from 0.6 +/- 0.04 and 2.2 +/- 0.1 to 1.3 +/- 0.2 and 6.7 +/- 0.7 mmol/L, respectively. During reduced maternal uterine blood flow indomethacin caused a significantly greater increase in plasma glucose and lactate concentrations than the vehicle; plasma glucose and lactate concentrations increased to a maximum of 1.8 +/- 0.2 and 22.7 +/- 0.8 mmol/L, respectively, during indomethacin infusions compared with 1.1 +/- 0.1 and 15.7 +/- 1.7 mmol/L, respectively, during vehicle infusions. The addition of prostaglandin E2 to the indomethacin infusion prevented the enhanced increase in glucose and lactate concentrations during reduced maternal uterine blood flow and caused a significant increase in fetal plasma insulin concentrations from 12.6 +/- 0.7 to 60.9 +/- 28.1 microU/ml. CONCLUSION: The inhibition of prostaglandin synthesis during fetal hypoxemia alters the metabolic response of the fetus, leading to a severe metabolic acidosis.     

Dehydration increases the renal response to atrial natriuretic peptide in fetal sheep.

OBJECTIVE: In sheep, maternal water deprivation results in urinary natriuresis in spite of suppression of plasma atrial natriuretic factor levels. Near-term fetal sheep also have a urinary natriuresis without change in plasma atrial natriuretic factor during maternal dehydration. This study was designed to explore the role of plasma atrial natriuretic factor levels in fetal dehydration-natriuresis. STUDY DESIGN: Eight chronically instrumented preterm (113 +/- 1 days) ovine fetuses received two atrial natriuretic factor infusions (3 and 15 ng/kg/min) in a euhydrated state and after 48 +/- 1 hours of maternal water deprivation. RESULTS: Dehydration significantly increased maternal plasma osmolality (302 +/- 2 to 313 +/- 2 mOsm/kg water), sodium (148.1 +/- 0.8 to 154.3 +/- 0.4 mEq/L), chloride (112.4 +/- 0.6 to 116.8 +/- 0.9 mEq/L), and arginine vasopressin (4.2 +/- 1.2 to 23.0 +/- 4.0 pg/ml) and significantly decreased plasma atrial natriuretic factor (36 +/- 6 to 19 +/- 4 pg/ml) concentrations. Fetal plasma osmolality (296 +/- 1 to 308 +/- 2 mOsm/kg), atrial natriuretic factor (128 +/- 16 to 241 +/- 36 pg/ml), and arginine vasopressin (3.5 +/- 0.8 to 12.3 +/- 4.8 pg/ml) concentrations and urine osmolality (170 +/- 10 to 253 +/- 10 mOsm/kg), osmolar clearance (0.80 +/- 0.02 to 0.14 +/- 0.02 ml/kg/min), and fractional sodium excretion (3.3% +/- 1.7% to 8.5% +/- 2.1%) increased significantly with dehydration, whereas the plasma atrial natriuretic factor clearance decreased from 127 +/- 27 to 63 +/- 10 ml/kg/min. Dehydration had no effect on fetal hematocrit, vascular pressures, glomerular filtration rate, urine flow, or free water clearance. In euhydrated fetuses plasma atrial natriuretic factor increased from 128 +/- 16 to 287 +/- 46 pg/ml with sequential atrial natriuretic factor infusion, and no significant increases were observed in urine flow, fractional sodium excretion, and glomerular filtration rate. In contrast, atrial natriuretic factor infusion to dehydrated fetuses significantly increased urine flow (0.17 +/- 0.03 to 0.32 +/- 0.07 ml/kg/min), osmolar clearance (0.14 +/- 0.02 to 0.28 +/- 0.06 ml/kg/min), and fractional sodium excretion (8.5% +/- 2.1% to 14.8% +/- 4.0%). CONCLUSION: These results demonstrate that in the fetus at 113 days' gestation plasma atrial natriuretic factor levels increase with dehydration, probably a result of decreased plasma atrial natriuretic factor clearance, and the fetal renal responsiveness to atrial natriuretic factor infusion increases during maternal dehydration.     

Doppler assessment of fetal blood flow velocity waveforms during acute maternal oxygen administration as predictor of fetal outcome in post-term pregnancy

The changes in fetal blood flow velocity waveforms during maternal administration of 60% humidified oxygen were assessed by Doppler ultrasonography in 45 post-term fetuses. During oxygen treatment, nine fetuses exhibited temporary increases (24.3 +/- 2.0% [1 standard deviation] above pretreatment values) in the pulsatility index at the level of internal carotid artery. Although no significant changes (2.9 +/- 5.1%) were found in the remaining 36 fetuses. In this former group a higher incidence of emergency cesarean delivery due to fetal distress and more neonatal complications were observed. Also, meconium staining of the amniotic fluid and low 1- and 5-minute Apgar scores occurred more frequently in the group of fetuses who responded to maternal oxygen administration. An increase of at least 20% in the pulsatility index of internal carotid artery during maternal hyperoxygenation may be a useful marker of adverse outcome in post-term fetuses.     

Fetal hemodynamic response to maternal intravenous nicotine administration.

OBJECTIVES: Our study was designed to test the hypothesis that maternally administered nicotine has significant effects on fetal hemodynamics and umbilical systolic/diastolic ratios. STUDY DESIGN: Nine pregnant ewes received maternal intravenous infusions of 10, 20, and 30 micrograms/kg/min of nicotine. Maternal and fetal blood pressure, heart rate, and uterine and umbilical blood flow were recorded. RESULTS: Maternal intravenous administration of nicotine (10, 20, and 30 micrograms/kg/min of maternal body weight) produced significant (p < 0.05) increases in fetal blood pressure (2%, 11%, and 25%, respectively), decreases in fetal heart rate (0%, 8%, and 12%), and decreases in umbilical blood flow (0%, 0%, and 19%). Umbilical systolic/diastolic ratios increased slightly at the 30 micrograms/kg/min dose of nicotine, but these changes did not reach significance. Maternal blood pressure increased (10%, 25%, and 53%), and uterine vascular resistance increased (5%, 64%, and 344%) significantly (p < 0.05); uterine blood flow increased at the 10 micrograms/kg/min dose (+5%) and decreased by 23% and 42% at the highest two doses of nicotine. CONCLUSION: Maternal nicotine administration in late-term pregnant sheep produced significant increases in fetal arterial blood pressure and umbilical vascular resistance, decreased fetal heart rate, and umbilical blood flow but did not significantly alter systolic/diastolic ratios.     

Fetal cardiorespiratory changes during spontaneous prelabor uterine contractions in sheep

Fetal cardiorespiratory changes during spontaneous prelabor uterine contractions (called contractures) were studied in 12 chronically catheterized fetal sheep at 120 to 143 days' gestation. During contractures the carcass blood flow increased significantly from 27 +/- 2 (SEM) to 32 +/- 3 ml/min/100 gm. There were no significant changes in combined ventricular output or in blood flow to the umbilical circulation, brain, heart, adrenal glands, gut, kidney, and lung. Fetal arterial blood pressure increased from 57 +/- 2 to 62 +/- 1 mm Hg (p less than 0.001) during contractions. There were no significant changes in fetal heart rate. In the fetal femoral artery during contractures the oxygen content decreased from 6.1 +/- 0.2 to 5.4 +/- 0.2 ml/dl of blood (p less than 0.001), and carbon dioxide tension increased significantly from 44 +/- 0.4 to 45 +/- 0.4 mm Hg (p less than 0.001). The pH did not change. The increase in carcass blood flow during contractures suggests that there was an increase in fetal skeletal muscular activity or tone. An increase in fetal skeletal muscle activity, together with a decrease in uterine blood flow could explain the small decrease in fetal oxygen content that occurs with each contracture. Fetal compression and/or changes from rapid eye movement to synchronized sleep or arousal observed during contractures are possible stimuli causing increased fetal skeletal muscle tone or activity. Since contractures periodically result in neuromuscular activity in the fetus in its protected fluid-filled environment, they may play a key role in fetal neuromuscular development by stimulating "exercising" in the fetus in utero.