Fetal hypertension induced by norepinephrine infusion and umbilical artery flow velocity waveforms in fetal sheep

This study was designed to examine the effects of fetal hypertension on the umbilical artery pulsatility index. Fetal arterial blood pressure and umbilical venous pressure were measured in eight sheep, 3 to 5 days after surgery. Umbilical blood flow was measured with an electromagnetic flowmeter around the common umbilical vein. Umbilical artery flow velocity waveforms were obtained either by an indwelling 5 MHz pulsed Doppler device (n = 4) or transcutaneously by a 4 MHz continuous-wave Doppler device (n = 4). Fetal blood pressure was raised by intravenous infusion of norepinephrine 10 micrograms/min during 5 minutes. Norepinephrine infusion resulted in elevated arterial and umbilical venous pressures, accompanied by a bradycardia during the first 3 minutes. Umbilical blood flow, calculated placental vascular resistance, and umbilical artery pulsatility index did not change. After atropine administration, the norepinephrine-induced elevated arterial and umbilical venous pressures were accompanied by tachycardia, increased umbilical blood flow, and no change in placental vascular resistance and umbilical artery pulsatility index. It is concluded that fetal arterial hypertension provoked by norepinephrine infusion has no effect on placental vascular resistance, umbilical blood flow, and umbilical artery pulsatility index.     

The acute response of the umbilical artery pulsatility index to changes in blood volume in fetal sheep.

This experimental study was designed to test the effects of acute changes in fetal circulating blood volume on the umbilical artery pulsatility index (PI). Six fetal sheep were provided with an electromagnetic flow meter for measurement of umbilical venous blood flow, with catheters for determination of arterial blood pressure and umbilical venous pressure, and with a 5 MHz Doppler transducer around one umbilical artery for flow velocity waveform analysis. A catheter in the inferior vena cava was used to infuse 50 ml of maternal blood (hypervolemia) into the fetal circulation or to withdraw 50 ml of fetal blood (hypovolemia) after volume correction. Hypervolemia resulted in a rise in arterial pressure and umbilical venous pressure, without an effect on PI, umbilical blood flow or placental vascular resistance. Hypovolemia resulted in a decrease in fetal heart rate, arterial pressure, umbilical venous pressure and umbilical blood flow. Calculated placental vascular resistance was not changed, whereas the PI increased by 42%. We conclude that volume loading with 10-15% of fetal circulating volume does not affect the umbilical artery PI, whereas acute reduction of fetal blood volume with the same amount is associated with an increase in the umbilical artery PI, without changes in calculated placental vascular resistance.     

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.     

Venous Doppler velocimetry in relationship to central venous pressure and heart rate during hypoxia in the ovine fetus.

OBJECTIVE: Characteristic changes in ductus venosus (DV) blood velocity and pulsations in the umbilical vein (UV) have been described during imminent fetal asphyxia. The aim of this study was to examine fetal venous blood velocity in relationship to pressure gradient across the DV during hypoxia in a fetal lamb preparation. METHODS: In general anesthesia, a cesarean section was performed on seven pregnant ewes, the fetus was exteriorized and put into a heated waterbath with uninterrupted umbilical circulation. Pressure measurements in the UV and inferior vena cava (IVC) were performed with the catheter tips on both sides of the DV. Fetal hypoxemia was induced by giving the ewe 12% oxygen in inhaling air. Pressure across the DV and Doppler velocimetry were repeatedly measured during hypoxemia. Blood velocity was recorded in the DV and UV by Doppler ultrasound. RESULTS: Before hypoxia the median pressure gradient across the DV was in systole 1 mmHg and 0.31 mmHg in end-diastole and during hypoxemia 1.5 mmHg and zero, respectively. The pressure difference across the DV was constant during hypoxemia irrespective of the presence of umbilical venous pulsations or heart rate. IVC-pressure was greatly influenced by fetal heart rate (FHR). A small but linear fall in systolic IVC pressure was seen with increasing FHR. In end-diastole the IVC pressure changed in a parabolic fashion, with increasing pressure during brady- and tachycardia. Pulsations in the UV also showed a parabolic relationship to FHR and central venous pressure. DV end-systolic and end-diastolic blood velocity changed during hypoxemia in direct relationship to FHR and central venous pressure, but without direct relationship to fetal blood gases. CONCLUSION: The pressure gradient across the DV is constant during hypoxemia. Changes in central and umbilical venous pressure are directly related to FHR. Umbilical venous and DV blood velocity changed in direct relationship to FHR and central venous pressure.     

Effects of fetal breathing movements on umbilical venous blood flow in fetal lambs

The effects of fetal breathing movements on the blood flow pattern in the common umbilical vein were studied in six chronically instrumented fetal lambs between 106 and 143 days gestation. Umbilical venous blood flow was measured with an electromagnetic flow transducer around the intra-abdominal common umbilical vein. Fetal breathing movements were recorded by means of an intratracheal catheter. During rapid irregular breathing movements instantaneous umbilical venous blood flow showed undulations with the frequency of the breathing movements. An inspiratory movement, characterized by a fall in tracheal pressure (mean +/- S.D. = 5.3 +/- 1.7 mmHg) was accompanied by a decrease in instantaneous umbilical venous blood flow (mean +/- S.D. = 10.5 +/- 2.8%). This decrease in umbilical blood flow during inspiration was accompanied by an increase in intra-abdominal pressure. A much greater decrease (mean +/- S.D. = 40.6 +/- 18.4%) in instantaneous umbilical venous blood flow occurred during deep inspiratory efforts (mean pressure drop +/- S.D. = 15.5 +/- 4.3 mmHg), accompanied by marked increases in intra-abdominal pressure. Isolated expiratory efforts resulted in an increase in both tracheal (mean +/- S.D. = 6.3 +/- 2.6 mmHg) and intra-abdominal pressure, while umbilical venous blood flow decreased (mean +/- S.D. = 33.5 +/- 21.3%). These observations show the great influence of fetal respiratory movements on the blood flow pattern in the common umbilical vein. The changes in instantaneous umbilical venous blood flow are possibly brought about by changes in intra-abdominal pressure.     

Association of umbilical venous with inferior vena cava blood flow velocities

The fetal cardiac and placental circulations are interconnected through the umbilical venous and arterial vasculature. We hypothesized that alterations in umbilical venous blood flow velocities are present in fetuses with abnormal umbilical arterial circulation, and further, that changes in inferior vena cava blood flow velocities occur with, and might explain, these variations in umbilical venous blood flow velocities. Umbilical venous and inferior vena cava blood flow velocities were examined in 15 normal fetuses and in 59 fetuses with abnormalities that included absent end-diastolic umbilical artery blood flow velocities (N = 21) or abnormal heart rates (N = 27). Inferior vena cava velocities were also analyzed in 11 other fetuses with anomalies or known growth or placental abnormalities who had abnormal umbilical venous blood flow velocities. In normal fetuses, variations in umbilical venous velocities occurred during fetal activity or with fetal breathing; however, no variation in velocity corresponded with heart rate. Eleven of 21 fetuses with absent end-diastolic velocities in the umbilical artery demonstrated decreases in umbilical venous velocities ("venous pulsations") during arterial diastole. Blood flow velocities in the reverse direction, from the right atrium into the inferior vena cava with atrial contraction, were significantly greater in these fetuses than in those without umbilical venous pulsations (27.5 +/- 14.9% and 7.5 +/- 5.7% of total forward flow velocity, respectively; P less than .001). Venous pulsations were also seen in fetuses with abnormally fast or slow heart rates; reverse flow with atrial contraction in the inferior vena cava was likewise greater than normal in these fetuses.(ABSTRACT TRUNCATED AT 250 WORDS)     

Umbilical artery and uteroplacental blood flow velocity waveforms in normal pregnancy--a cross-sectional study

Umbilical and arcuate artery blood flow velocity waveforms (FVW) were recorded in 125 normal singleton pregnancies from 20 to 42 weeks of gestation. The FVW were analysed for pulsatility index (PI), peak systolic velocity/minimum diastolic velocity ratio (S/D ratio), rising slope (RS) and descending slope (DS). Both in the umbilical and arcuate arteries, values for all variables declined with advancing gestation, indicating decreasing placental vascular resistance. The umbilical artery PI was unaffected by the fetal heart rate, but the arcuate artery PI was negatively correlated to the maternal heart rate (r = -0.40). The arcuate artery PI decreased by 0.00394 with each beat per minute increase in maternal heart rate. Normal limits (mean +/- 2 SD) were established for umbilical artery PI corrected for gestational age, and arcuate artery PI corrected for gestational age and maternal heart rate.     

Pulsatility index and its relationship to placental vascular resistance during partial umbilical venous occlusion: a study in fetal lambs

To study the effect of partial occlusion of the umbilical vein upon umbilical artery velocity waveforms, 4 chronically instrumented pregnant sheep have been subjected to measurement of the relevant haemodynamic parameters, i.e. the arterial inflow pressure, placental venous outflow pressure (Pv), venous blood flow (Quv) and arterial blood velocity waveform. The pulsatility index (PI) of the velocity waveform increases significantly for a Quv reduction of 40% or more (p less than 0.05). The Quv correlates well with the PI (r = 0.61) and the Pv (r = 0.71). The correlation between fetal heart rate (FHR) and Quv, FHR and PI is 0.75 and 0.64, respectively. The placental vascular resistance (R) can be calculated using the Poiseuille equation. There is not significant correlation between R and PI. It can be concluded that the increase in PI in the umbilical artery during partial venous occlusion is very likely caused by an increased Pv rather than a change in R.     

Fetal infusions of plasma cause an increase in umbilical vascular resistance in sheep

Earlier studies suggested that the fetal placental circulation is relatively inert with fetal placental flow increasing or decreasing with perfusion pressure. Subsequent studies have demonstrated that the placenta may not be an unreactive vascular bed. The present study was undertaken to determine if plasma infusion-induced hypertension increased fetal placental flow in proportion to the driving pressure across the fetal placental circulation. Six fetal sheep were operated on at 118-122 days to place intravascular catheters and a flow sensor on the common umbilical artery. Starting 6 days later, the fetuses were infused with adult sheep plasma. During the 7-day-long infusion period, they received a total of 1515+/-217 (SD) ml of fluid and 93.2+/-12.0 g of protein. Fetal plasma protein concentrations increased from 34.2+/-2.3 to 77.0+/-9.7 g/l (P<0.0001). Fetal arterial blood pressures rose from 42+/-3 to 59+/-4 mmHg (P<0.01) and venous pressures rose from 2.2+/-0.5 to 4.8+/-0.8 mmHg (P<0.01). In spite of the large increase in driving pressure, fetal placental blood flow remained (statistically) constant (627+/-299 ml/min and 552+/-221 ml/min) while fetal umbilical resistance increased from 0.077+/-0.038 to 0.115+/-0.053 mmHg min/ml (P<0.01). On day 7, plasma renin activity had fallen from 6.7+/-4.2 ng/(ml/h) at preinfusion control to 0.6+/-0.6 ng/(ml/h) (P<0.05) and plasma angiotensin-II concentration had fallen from 33.2+/-26.6 to 6.2+/-3.9 pg/ml, although this fall was not statistically significant (P=0.07). Fetal placental flow did not increase with increased driving pressure across the fetal placental circulation. The increase in fetal placental resistance may be a response to the increase in arterial pressure since there was no increase in flow.     

Effects of dexamethasone on the uterine and umbilical vascular beds during basal and hypoxemic conditions in sheep

OBJECTIVE: The purpose of the study was to test the hypotheses that maternal treatment with dexamethasone leads to a reduction in basal umbilical blood flow and diminishes the fetal umbilical hemodynamic response to acute hypoxemic stress in sheep. STUDY DESIGN: While under general anesthesia, 23 ewes and their fetuses were instrumented with vascular catheters and transonic blood flow probes around a uterine and umbilical artery at 117 days of gestation (term, approximately 145 days). At 124 days, the ewes were injected intramuscularly with 2 doses of either dexamethasone (12 mg) or saline solution at 24-hour intervals. All animals experienced 2 episodes of hypoxemia during treatment (125+/-1 days) and after treatment (128+/-1 days). RESULTS: Maternal dexamethasone treatment caused a sustained increase in fetal arterial blood pressure (from 41+/-3 mm Hg to 45+/-3 mm Hg) and a transient fall in umbilical vascular conductance (from 6.2+/-0.9 mL. min(-1). [mm Hg](-1) to 5.4+/-0.7 mL. min(-1). [mm Hg](-1)). During both episodes of hypoxemia, there was a significant increase in umbilical blood flow in the controls, but not in the dexamethasone-treated animals. CONCLUSION: Maternal dexamethasone treatment with doses used in human clinical practice significantly decreased basal umbilical vascular conductance and prevented the normal increase in umbilical blood flow that is induced by acute hypoxemia in fetal sheep.     

Doppler measurements of blood flow velocity and waveforms in fetal venous circulation

Ultrasonic velocimetry of the fetal circulation became a very useful method in assessment of fetal well-being, especially in high risk pregnancies. There are many papers concerning on distribution and regulation of blood flow in umbilical artery, middle cerebral artery, and much less dealing with flow velocity waveforms in inferior vena cava and ductus venosus and their clinical significance. Fetal compromise is associated with significant alterations in the fetal arterial and venous circulation. Changes in venous Doppler waveforms develop due to increased afterload and perhaps myocardial failure in deterioration after arterial redistribution is established. Doppler investigation of the fetal venous circulation may play an important role in monitoring the redistribution and may help to determine the optimal time for delivery.     

Redistribution of power spectrum of heart rate variability during acute umbilical artery embolism and hypoxemia in late-gestation fetal sheep

OBJECTS: Fetal heart rate variability (HRV) is subject to a number of factors, including fetal distress. The aim of this study was to investigate the power spectral distribution of fetal heart rate variability during acute hypoxemia following umbilical artery embolism and to test the hypothesis that the relative proportion of frequency domains in total power of HRV, reflects the changes in HRV during hypoxemia more closely than the absolute values. METHODS: Acute hypoxemia was induced in seven catheterized late-gestation fetal sheep by repeated injections of microspheres to cause umbilical artery embolism. The very-low, low-, middle- and high-frequency domains (0-0.025, 0.025-0.125, 0.125-0.20, and 0.20-0.50 cycles/beat, respectively) were determined by power spectral analysis. RESULTS: Umbilical artery embolism induced marked fetal hypoxemia, hypercapnia and acidosis, accompanied by an increase in heart rate and a decrease in arterial blood pressure. These changes were associated with the increase in power over the entire frequency range and in the relative power in the low-frequency range (P<0.01), and with decrease in the relative power in the high-frequency range (P<0.05). Correlations were found between the relative power in the low- and high-frequency ranges and PO2 and between the relative power in these ranges and mean arterial blood pressure (P<0.05), but not PCO2 or pH. CONCLUSIONS: The present study indicates that acute hypoxemia induced by umbilical artery embolism leads to the redistribution of power spectral density of fetal HRV and that the relative proportion of individual frequency domains may reflect the changes in HRV during acute hypoxemia more closely than the absolute power values.     

Maternal and fetal plasma endothelin levels in intrauterine growth restriction: relation to umbilical artery Doppler flow velocimetry

The objective of this study was to examine maternal and fetal endothelin-1 (ET-1) in pregnancies complicated with intrauterine growth restriction (IUGR) and to correlate these data with umbilical artery Doppler flow velocity waveforms (FVW). Higher mean maternal (13.8 +/- 6.4 vs 9.2 +/- 3.4 pmol/L, p < 0.05) and fetal (18.5 +/- 9.6 vs 11.7 +/- 6.9 pmol/L, p < 0.05) ET-1 levels were found in pregnancies complicated with IUGR than in controls. Fetal ET-1 level was related to birth weight percentile for gestational week. Maternal and fetal ET-1 concentrations were not related to umbilical artery Doppler flow S/D ratio, PI and RI. Maternal or fetal ET-1 concentrations were also not related to umbilical artery pH, PO2 and PCO2. Pregnancy-induced hypertension was significantly associated with an elevated fetal and maternal ET-1 concentration. In conclusion, increased production and secretion of ET-1 may play a role in the pathophysiology of idiopathic IUGR. Over-production of ET-1 in IUGR is not associated with increased placental resistance as reflected in abnormal umbilical artery Doppler FVW.     

Effect of endothelium-derived relaxing factor inhibition on the umbilical-placental circulation in fetal lambs in utero.

OBJECTIVE: The purpose of this study was to examine whether basal endothelium-derived relaxing factor release contributes to regulation of resting umbilical-placental vascular resistance. STUDY DESIGN: Because N omega-nitro-L-arginine selectively inhibits the synthesis of nitric oxide, a major endothelium-derived relaxing factor, we investigated the effects of N omega-nitro-L-arginine on umbilical-placental vascular resistance in 10 fetal lambs in utero. We inserted catheters and fitted an umbilical artery electromagnetic flow transducer around the common umbilical artery to measure umbilical blood flow and catheterized the left umbilical arterial hypogastric branch to allow selective umbilical-placental infusion (60 minutes) of pH-matched saline solution (control) or N omega-nitro-L-arginine. RESULTS: In seven normal fetal lambs, N omega-nitro-L-arginine increased umbilical-placental vascular resistance and arterial pressures and decreased umbilical blood flow (p less than 0.05); percentage changes from baseline were 50.8% +/- 18.3%, 40.3% +/- 8.1%, and -9.9% +/- 6.4%, respectively. In three mildly asphyxiated (compromised) fetuses, these changes were 101.4% +/- 28.7%, 31.2% +/- 4.8%, and -37.9% +/- 12.0%. CONCLUSION: These data support the hypothesis that the basal endothelium-derived relaxing factor release plays a role in regulating resting umbilical-placental vascular resistance.     

The effects of low-dose endotoxin on the umbilicoplacental circulation in preterm sheep

OBJECTIVE: In the present study we examined the effects of low-dose endotoxin (lipopolysaccharides, LPS) on continuously recorded umbilical blood flow. METHODS: Twenty fetal sheep were catheterized at a gestational age of 107 +/- 1 days. A flow probe was placed around either the common umbilical artery or one single umbilical artery. Three days later fetuses received either 100 or 500 nanograms of LPS (n = 14) or 2 mL saline (n = 6) intravenously. Six fetuses died within 12 hours after LPS. Fetal heart rate (FHR), mean arterial pressure (MAP), and umbilical blood flow (Q(umb)) were monitored for 3 days. RESULTS: FHR increased by 25 +/- 4% at 4-5 hours after LPS (P <.01) and was elevated for 15 hours after LPS. MAP increased by 18 +/- 5% 1 hour after LPS (P <.01) and returned to control value 4-5 hours after LPS. Q(umb) began to decrease 1 hour after LPS and was minimal (-30 +/- 7%, P <.001) at 4-5 hours after LPS. Q(umb) slowly returned to the control value at 12 hours after LPS. Placental vascular resistance increased by 73 +/- 37% (P <.01), whereas pH did not appreciably change. CONCLUSION: Intravenous application of endotoxin caused a substantial and long-lasting decrease in umbilical blood flow resulting in fetal hypoxemia without acidemia. These effects may be of significance in the development of fetal brain damage associated with intrauterine infection.     

Phasic blood flow patterns in the common umbilical vein of fetal sheep during umbilical cord occlusion and the influence of autonomic nervous system blockade

The blood flow pattern in the common umbilical vein is under normal conditions nonpulsatile in contrast to the flow in the fetal inferior vena cava. We observed pulsatile flow patterns in the common umbilical vein of fetal lambs during changes in the fetal hemodynamic equilibrium. These pulsations may influence the mixing of oxygen-rich ductus venosus blood and oxygen-poor inferior vena cava blood. This study deals with the phasic changes in umbilical venous blood flow during cord occlusion. The experiments were performed in eight chronically instrumented fetal lambs between 114 and 133 days gestation (term 146 days). Umbilical venous blood flow was measured with an electromagnetic flow transducer around the intraabdominal common part of both umbilical veins. The fetuses were provided with catheter in the fetal abdominal aorta and with electrodes for monitoring arterial blood pressure and heart rate. Occlusion of the umbilical cord was performed by means of an inflatable balloon occluder around the total cord (occlusion time 20 to 90 seconds). Occlusions were performed in fetuses with an intact autonomic nervous system and after blockade of the alpha-adrenergic, beta-adrenergic or cholinergic part of the autonomic nervous system.     

Behavior-state–dependent changes in human fetal pulmonary blood flow velocity waveforms

Objective: To establish the influence of fetal behavior states on venous and arterial pulmonary blood flow velocity waveforms in the normally developing term fetus.Methods: The relation between venous and arterial pulmonary blood flow velocity waveforms and fetal behavior states was investigated in 18 normal term fetuses. Recordings of the venous pulmonary blood flow velocity waveforms were obtained just proximal to the entrance in the left atrium, and the arterial pulmonary blood flow velocity waveforms were taken from the most proximal branch of the pulmonary artery in the same lung using color Doppler imaging. Time-averaged peak systolic, peak diastolic, and end-diastolic flow velocity; peak systolic to peak diastolic ratio; pulsatility index; and fetal heart rate were calculated from both venous and arterial Doppler recordings obtained during behavior states 1F (quiet sleep) and 2F (active sleep). Fetal behavior states were determined from combined recordings of fetal eye and body movements.Results: Recordings of sufficient quality for analysis were obtained from ten fetuses. Venous pulmonary blood flow velocity waveforms demonstrated a statistically significant increase in time-averaged peak diastolic and end-diastolic velocity during fetal behavior state 2F. No behavior-state-related changes were observed for the arterial pulmonary blood flow velocity waveform.Conclusion: The data suggest an increased pressure gradient between the pulmonary venous system and the left atrium during behavior state 2F. Flow velocity waveforms from the proximal arterial pulmonary branch are independent of behavioral state.     

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.     

Doppler velocimetry and fetal heart rate studies in nephropathic diabetics.

OBJECTIVES: Our objectives were to determine in pregnancies complicated by diabetic nephropathy (1) if impedance to flow in the uterine and umbilical arteries is normal and (2) if these fetuses are hypoxemic and acidemic and if they have decreased fetal heart rate variation and Doppler blood flow redistribution. STUDY DESIGN: In a cross-sectional study at the Harris Birthright Research Centre for Fetal Medicine, London, serial assessment of fetal heart rate variation and Doppler velocimetry of the placental and fetal circulations was undertaken in six pregnancies complicated by diabetic nephropathy. In all cases cordocentesis was performed within 24 hours before delivery for the measurement of umbilical venous blood gases. RESULTS: Cordocentesis demonstrated these fetuses to be hypoxemic and acidemic. The fetal heart rate variation was decreased; however, impedance to flow in the uterine artery was normal, and increased impedance to flow in the umbilical artery with evidence of blood flow redistribution was observed in only one case. CONCLUSIONS: Fetal hypoxemia and acidemia in pregnancies complicated by diabetic nephropathy is not a consequence of impaired placental perfusion, and the degree of metabolic derangement may be obscured by the apparent normal growth and failure of these fetuses to demonstrate blood flow redistribution.     

Direct determination of the ovine fetal umbilical artery blood flow waveform

Ultrasonographic umbilical artery blood flow velocity waveform analysis has been proposed as a means of noninvasive assessment of fetal well-being. We computed waveform indices from directly measured umbilical artery blood flow in chronically instrumented ovine fetuses from 109 to 138 days of gestation (term, 145 days). The three waveform indices (systolic/diastolic ratio, pulsatility index, and resistance index) correlated significantly with each other (r = 0.90 to 0.98). These indices progressively decreased with gestation and were significantly correlated with calculated umbilical vascular resistance (r = 0.68 to 0.70, p less than 0.01) and with umbilical blood flow (r = -0.71, p less than 0.01). During the final week of pregnancy, systolic/diastolic ratio could be predicted by the combination of placental size (total cotyledonary mass), fetal size (ponderal index), and either umbilical blood flow or umbilical vascular resistance (multiple linear regression, r2 = 0.94). Fetal heart rate declined from day 109 of gestation to 138 days. Fetal heart rate was significantly correlated with waveform indices only when values exceeded 170 beats/min (r = -0.37 to -0.51). Ovine fetal umbilical artery waveform indices changed at approximately the same rate as those reported for human fetuses in late gestation on the basis of external Doppler ultrasonographic velocity measurements. These results suggest that the sheep is a suitable model for investigations of umbilical artery waveform analysis.