-
[show abstract]
[hide abstract]
ABSTRACT: Our purpose was to examine regulatory linkages between fetal oxygenation and fetal and placental growth. We determined umbilical cord PO (2) and oxygen saturation, fractional oxygen extraction, and birth to placental weight ratio values in relation to size at birth for a large tertiary hospital population delivering at term.
The computerized perinatal database of St Joseph's Health Care London, London, Ontario, was used to obtain the umbilical cord gases, pH, birth weight, placental weight, and other selected information for all term, singleton, liveborn infants between January 1990 and December 1999 (N = 27,043). Oxygen saturation values were calculated from the umbilical cord PO(2) and pH data with a previously derived empirical equation; fractional oxygen extraction values were calculated from the umbilical cord oxygen saturation data. Size at birth was divided into the following 5 birth weight categories using neonatal growth standards: fetal growth restriction, <3%; borderline fetal growth restriction, >or=3% and <10%; appropriate for gestational age, >or=10% and <or=90%; borderline large for gestational age, >90% and <or=97%; large for gestational age, >97%.
Infants in the borderline fetal growth restriction and fetal growth restriction groups had umbilical vein and artery PO(2) and oxygen saturation values that were stepwise lower than respective values for infants in the appropriate for gestational age group. Conversely, infants in the borderline large for gestational age and large for gestational age groups had umbilical vein PO(2) and oxygen saturation values that were stepwise higher than respective appropriate for gestational age group values; infants in these groups showed no change in arterial PO (2) and oxygen saturation values. Therefore infants in the borderline fetal growth restriction and fetal growth restriction groups had fractional oxygen extraction values that were stepwise higher than the appropriate for gestational age group value, whereas values for infants in the borderline large for gestational age and large for gestational age groups remained unchanged. Birth weight was disproportional to placental weight for infants in the borderline fetal growth restriction and fetal growth restriction groups when compared with that of the infants in the appropriate for gestational age group, with the birth to placental weight ratio values stepwise decreased. Conversely, birth weight was proportional to placental weight for infants in the borderline large for gestational age and large for gestational age groups with the birth to placental weight ratio values thus unchanged when compared with that of the infants in the appropriate for gestational age group.
We conclude that fetal oxygenation is related to size at birth across the entire range of birth weights as studied at term from macrosomic to growth-restricted infants; this conclusion supports oxygen as a primary determinant of fetal growth. However, there are differences in the linkage between fetal oxygenation and metabolic rate or growth for these cohort groups that may relate to underlying etiologic processes.
American Journal of Obstetrics and Gynecology 09/2001; 185(3):674-82. · 3.47 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: The aim of this study was to test the null hypothesis that size at birth relative to fetal or neonatal growth standards is not a significant variable related to the risk of spontaneous preterm delivery.
This was a hospital-based cohort study of consecutive births at a tertiary care perinatal center from January 1, 1985, to December 31, 1996. A total of 37,377 pregnancies met the following inclusion criteria: (1) singleton gestation, (2) 25 to 40 weeks' gestation, and (3) no anomalies. Neonates were divided into 5 birth weight categories according to either fetal (uncorrected for sex) or neonatal (corrected for sex) growth standards, as follows: (1) intrauterine growth restriction, birth weight <3rd percentile; (2) borderline intrauterine growth restriction, birth weight > or = 3rd percentile and <10th percentile; (3) appropriate for gestational age, birth weight from 10th percentile through 90th percentile; (4) borderline large for gestational age, birth weight >90th percentile but < or = 97th percentile, and (5) large for gestational age, birth weight >97th percentile. Logistic regression analysis was used to estimate the independent effect of birth weight category on the risk of preterm delivery after spontaneous onset of labor, with the appropriate-for-gestational-age group serving as a reference.
When fetal growth standards were applied, there was a significant increase in the risk of spontaneous preterm delivery when birth weight was outside the appropriate-for-gestational-age range (odds ratios of 2.5, 1.4, 1.2, and 1.9 for intrauterine growth restriction, borderline intrauterine growth restriction, borderline large-for-gestational age, and large-for-gestational-age groups, respectively). In contrast, when neonatal growth standards were applied, the risks of spontaneous preterm delivery in intrauterine growth restriction, borderline intrauterine growth restriction, and large-for-gestational-age groups were significantly lower (odds ratios of 0.5, 0.7, and 0.7 for intrauterine growth restriction, borderline intrauterine growth restriction, and large-for-gestational-age groups, respectively) because of an underestimation in the number of fetuses with abnormal size at birth delivered prematurely. With both fetal and neonatal growth standards there was a 5-to 6-fold greater risk of perinatal death for both preterm and term fetuses with intrauterine growth restriction.
Fetal growth standards are more appropriate in predicting the impact of birth weight category on the risk of spontaneous preterm delivery than are neonatal growth standards. When fetal standards are applied, the risks of preterm birth in both extreme abnormal birth weight categories (intrauterine growth restriction and large for gestational age) are 2- to 3-fold greater than the risk among appropriate-for-gestational-age infants.
American Journal of Obstetrics and Gynecology 04/2001; 184(5):946-53. · 3.47 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: To test the hypothesis that chronic placental insufficiency resulting in fetal growth restriction causes an increase in fetal lung surfactant-associated protein (SP) gene expression, we embolized chronically catheterized fetal sheep (n = 6) daily using nonradioactive microspheres in the abdominal aorta for 21 days (between 0.74 and 0.88 of gestation) until fetal arterial oxygen content was reduced by approximately 40-50%. Control animals (n = 7) received saline only. Basal fetal plasma cortisol concentration was monitored. At the end of the experiment, fetal lung tissues were collected, and ratios of tissue levels of SP-A, SP-B, and SP-C mRNA to 18S rRNA were determined by standard Northern blot analysis. Total DNA content of fetal lungs was reduced by 30% in the embolized group compared with control group (P = 0.01). There was a 2.7-fold increase in fetal lung SP-A mRNA (P < 0.05) and a 3.2-fold increase in SP-B mRNA (P < 0.01) in the chronically embolized group compared with those in the control group. SP-A and SP-B mRNA tissue levels were highly correlated with the mean fetal plasma cortisol levels on days 20-21 (r = 0.90, P < 0.01 for SP-A mRNA and r = 0.94, P < 0.01 for SP-B mRNA). SP-C mRNA tissue levels were not significantly affected by placental insufficiency. We conclude that fetal growth restriction due to placental insufficiency is associated with alterations in fetal lung SP, suggesting enhanced lung maturation that was highly dependent on the degree of increase in fetal plasma cortisol levels.
The American journal of physiology 03/1999; 276(3 Pt 1):L459-65.
-
[show abstract]
[hide abstract]
ABSTRACT: We sought to determine umbilical cord oxygen saturation and fractional oxygen extraction values as measured at birth for a large tertiary hospital population and their predictive value for measures of acidosis.
The computerized perinatal database of St. Joseph's Health Centre, London, Ontario, was used to obtain the umbilical cord gases, pH, mode of delivery, gestational age at delivery, and nuchal cord status for all live-born infants >500 gm between January 1991 and December 1995 (n = 22,134). Oxygen saturation values were calculated from the umbilical cord PO2 and pH data with a previously derived empirical equation, the accuracy of which was rechecked with 100 consecutive cord blood samples where oxygen saturation values were both calculated and measured with a hemoximeter (r = 0.99, p = 0.001). Fractional oxygen extraction values were calculated from the umbilical cord oxygen saturation data.
There were 18,250 "validated" paired umbilical vein and artery blood gas and pH results available for analysis after patient case exclusions for missing, unreliable, or "unphysiologic" data. For all validated patient cases, mean umbilical vein oxygen saturation was 63% +/- 16% (SD), mean umbilical artery oxygen saturation was 24% +/- 15%, and mean fractional oxygen extraction was 0.62 +/- 0.20, with all three of these parameters significantly affected by mode of delivery, gestational age at delivery, and nuchal cord status. Umbilical vein and artery oxygen saturation and fractional oxygen extraction values showed significant relationships with umbilical artery base excess, albeit weak (r = 0.18 to 0.22), and pH (r = 0.46), which were best described using cubic regression models. Receiver-operator characteristic curve statistics for the prediction of acidosis at birth were also significant for all three of these parameters but lower when predicting metabolic versus mixed acidosis. However, all showed a poor positive predictive value for significant acidosis at birth, whether metabolic or mixed and regardless of the cutoff values used.
Umbilical cord oxygen saturation and fractional oxygen extraction values as measured at birth for a large tertiary hospital population indicate a decreased oxygen margin of safety for infants born postterm, by cesarean section after labor, and with a nuchal cord. However, these values have a limited relationship to measures of acidosis, which may have clinical implications for the usefulness of intrapartum pulse oximetry.
American Journal of Obstetrics and Gynecology 04/1998; 178(3):572-9. · 3.47 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: The present study was designed to examine the effects of chronic fetal placental embolization on the expression of 11beta-hydroxysteroid dehydrogenase (11beta-HSD) types 1 and 2, the intracellular enzymes responsible for the metabolism of glucocorticoids. Twelve instrumented fetal sheep were randomly allocated on Day 110 (term = 147 days) to either a control (n = 6) or embolized (n = 6) group. Embolized fetuses received daily injections of nonradioactive microspheres into the abdominal aorta for 21 days to decrease arterial oxygen content by 40-50% of the pre-embolization values. At the end of the experiment, fetal liver and kidney tissues as well as placental cotyledons were collected, and tissue levels of 11beta-HSD mRNA and activity were determined by standard Northern blot analysis and radiometric conversion assay, respectively. There was a 44% reduction (p < 0.01) in the level of renal 11beta-HSD2 mRNA in the embolized group as compared with the control group. Moreover, this reduction in mRNA was carried through to 11beta-HSD2 protein, since there was a corresponding decrease in the level of 11beta-HSD2 activity (4.5+/-0.2 vs. 2.9+/-0.1 pmol/min per milligram protein, p < 0.01). In contrast, levels of both 11beta-HSD1 mRNA and activity in the fetal liver remained unchanged. Moreover, both 11beta-HSD types 1 and 2 mRNA and activity in the placenta were not altered by the fetal placental embolization. In conclusion, chronic hypoxemia selectively inhibits renal 11beta-HSD2 mRNA expression and enzyme activity in the ovine fetus, which may contribute, at least in part, to the mechanisms leading to fetal hypertension.
Biology of Reproduction 01/1998; 58(1):234-9. · 4.01 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: To test the hypothesis that, in response to an increase in placental vascular resistance and progressive fetal asphyxia, the changes in external carotid blood flow waveforms are directly related to changes in external carotid vascular resistance, we embolized the fetal side of the placenta in pregnant sheep and measured cerebral and external carotid artery circulatory changes in relation to changes in external carotid artery flow waveforms. Chronically catheterized fetal sheep at 0.85 of gestation were embolized (n = 11) in the descending aorta for 6 h, until fetal arterial pH fell to approximately 6.90. Fetuses became rapidly hypoxemic (P < 0.0001) and developed a mixed respiratory and metabolic acidosis (P < 0.0001 for PCO2, pH, and base excess). There was a transient 40% increase in external carotid blood flow at pH approximately 7.25 and a parallel 32% increase in fetal arterial blood pressure (both (P < 0.01), whereas the external vascular resistance remained unaltered. Cerebral blood flow increased by 130% (P < 0.0001), and cerebral vascular resistance decreased by 125% (P < 0.0001) throughout the study. The external carotid resistance index (RI) decreased by 32% (P < 0.0001) at the time external carotid vascular resistance remained unchanged. This fall in external carotid RI was due almost entirely to a 110% increase in external carotid fundamental impedance (P < 0.001). We conclude that the poor relationship between the changes in external carotid vascular resistance and RI indicated that other hemodynamic factors such as vascular impedance to pulsatile flow must be measured for correct interpretation of changes in flow waveform shape under hypoxic conditions. In addition, changes in external carotid blood flow were not proportional to changes in cerebral blood flow in this model.
The American journal of physiology 10/1997; 273(4 Pt 2):H2001-8.
-
[show abstract]
[hide abstract]
ABSTRACT: Our purpose was to evaluate the predictive value of intrapartum fetal oxygen saturation as monitored by reflectance pulse oximetry (SpO2) for metabolic acidosis at birth.
An observational study was carried out on intrapartum patients at > or = 35 weeks' gestation having either a nonreassuring fetal heart rate pattern, intrauterine growth restriction, or thick meconium. Fetal oxygen saturation monitoring was performed with use of the Nellcor N-400 monitor and the FS-14 fetal oxygen sensor. Mean values of SpO2 from the last 30 minutes of monitoring were correlated with umbilical artery base excess and pH at birth, with use of regression analysis, whereas the prediction of acidosis by SpO2 at different thresholds was tested with use of receiver-operator characteristic curve calculations.
Fifty-four patients met the criteria for data analysis, with a mean SpO2 monitoring time of 150 +/- 124 minutes (SD) and a mean signal loss of 30% +/- 20%. Mean fetal SpO2 for the last 30 minutes of monitoring averaged 42.1% +/- 9.9% and, for individual patient studies, correlated significantly with calculated oxygen saturation in the umbilical vein (r = 0.52, p < 0.001) and in the umbilical artery (r = 0.34, p = 0.02) as measured at birth. However, the correlation with umbilical artery base excess values at birth was somewhat weaker (r = 0.30, p < 0.05), as was the correlation with umbilical artery pH values (r = 0.26, p = 0.05). Receiver-operator characteristic curve calculations were all nonsignificant when SpO2 from the last 30 minutes of monitoring was used as a diagnostic test for predicting acidosis at birth.
Intrapartum fetal SpO2 as monitored in the current study was of limited use as a diagnostic test for predicting acidosis at birth, regardless of the SpO2 cutoff value used.
American Journal of Obstetrics and Gynecology 10/1997; 177(4):775-9. · 3.47 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: The purpose of this study was to determine the endocrine and circulatory responses of the ovine fetus, near term, to sustained hypoxemic stress superimposed on chronic hypoxemia. Fetal sheep were chronically embolized (n = 7) for 10 days between 0.84 and 0.91 of gestation via the descending aorta until arterial oxygen content was decreased by approximately 30%. Control animals (n = 8) received saline only. On experimental day 10, both groups were embolized over a 6-h period until fetal arterial pH decreased to approximately 7.00. Regional distribution of lower body blood flows was measured on day 10, before and at the end of acute embolization. On day 10, the chronically embolized group had lower arterial oxygen content (P < 0.05), Po2 (P < 0.01), and placental blood flow (P < 0.05) than controls and higher prostaglandin E2 (PGE2) and norepinephrine plasma concentrations (both P < 0.05). In response to a superimposed sustained hypoxemic stress, there was a twofold greater increase in PGE2 in the chronically embolized group than in the control group (P < 0.05). However, the increase in fetal plasma cortisol in response to superimposed hypoxemic stress was similar in both groups, despite significantly lower adrenocorticotropic hormone and adrenal cortex blood flow responses in the chronically hypoxemic group (both P < 0.05). We conclude that PGE2 response to a sustained superimposed reduction in placental blood flow, leading to metabolic acidosis, is enhanced under conditions of chronic hypoxemia and may play an important role for the maintenance of the fetal cortisol response to an episode of superimposed acute stress.
The American journal of physiology 05/1997; 272(5 Pt 1):E817-23.
-
[show abstract]
[hide abstract]
ABSTRACT: Our purpose was to test the hypothesis that chronic placental insufficiency and intrauterine growth restriction in fetal sheep causes a decrease in the number of fetal heart rate accelerations and fetal heart rate variability.
Chronically catheterized fetal sheep were embolized (n = 6) daily with 15 to 50 microns latex microspheres for 21 days between 0.74 and 0.88 of gestation into the abdominal aorta, until fetal arterial oxygen content was decreased by 40% to 50% of the preembolization value. Control animals (n = 6) received saline solution only. Signals from chest electrodes were analyzed on-line with the Sonicaid System 8000 in 2-hour epochs every 6 hours starting at 8 AM over the first 48 hours of hypoxemia and for 2 hours between 8 and 10 AM every other day from day 3 to day 21 of hypoxemia. Umbilical artery Doppler-derived resistance index and fetal plasma catecholamine concentrations were also measured.
Embolized fetuses had asymmetric intrauterine growth restriction and became chronically hypoxemic (p < 0.001) with a progressive increase in the umbilical artery resistance index (p < 0.001). During the first 48 hours of hypoxemia the number of accelerations and decelerations and both short- and long-term fetal heart rate variability increased initially, followed by a return to control levels by 20 hours after the onset of embolization. After 21 days of hypoxemia the number of accelerations was significantly reduced by 30% compared with controls (p < 0.05). Both short- and long-term fetal heart rate variability in control fetuses gradually increased with advancing gestational age (p < 0.001 and p < 0.01, respectively), whereas in embolized fetuses the fetal heart rate variability remained unchanged and was 20% lower than that of controls on day 21 (both p < 0.01).
Intrauterine growth restriction and long-term hypoxemia in fetal sheep are associated with a decrease in short- and long-term fetal heart rate variability, possibly because of a delay in the normal maturational changes of the autonomic control of fetal heart rate.
American Journal of Obstetrics and Gynecology 03/1997; 176(2):282-90. · 3.47 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: To examine the cardiovascular effects on the fetus of an elevated umbilical vascular resistance resulting in fetal hypoxemia, we embolized the fetal side of the placenta in pregnant sheep and measured cardiovascular and hormonal changes and cellular growth in fetal heart. Chronically catheterized fetal sheep were embolized (n = 6) for 21 days between 0.74 and 0.88 of gestation into the descending aorta until arterial oxygen content was decreased by 40-50% of the preembolization value. Control animals (n = 6) received saline only. During embolization, fetuses became chronically hypoxemic (P < 0.001) and hypertensive (P < 0.001), with a progressive increase in umbilical artery resistance index (P < 0.001). There was also an increase in fetal plasma norepinephrine throughout the study period (P < 0.05). On day 21 of embolization, fetuses showed asymmetrical growth restriction, increased heart weight (P < 0.01), and increase in right and left ventricular wall thickness (P < 0.05) compared with control animals. The protein-to-DNA ratio, an index of cell size, increased in the right ventricular myocardium in the embolized group (P < 0.001), suggesting myocardial cell hypertrophy. We conclude that, during chronic placental damage leading to fetal hypoxemia with an increase in umbilical artery resistance index, fetuses developed arterial hypertension and asymmetrical growth restriction and that increases in afterload to the heart and plasma norepinephrine likely caused fetal myocardial hypertrophy.
The American journal of physiology 01/1997; 272(1 Pt 2):R201-7.
-
[show abstract]
[hide abstract]
ABSTRACT: The purpose of this study was to determine the cerebral, circulatory, and metabolic responses of the ovine fetus near term to umbilical cord compression with variable-type fetal heart rate decelerations.
Nine fetal sheep, at 0.9 of gestation, were studied before, during, and after umbilical cord occlusion for 1-minute and again after repetitive 1-minute cord occlusions every 5 minutes for 1 hour, with resultant fetal heart rate decelerations of approximately 90 beats/min. Brachiocephalic arterial and sagittal venous blood was analyzed for oxygen content, blood gases and pH, glucose, and lactate. Cerebral and upper body blood flow was measured with the microsphere technique.
Umbilical cord occlusion with moderate to severe variable-type fetal heart rate deceleration resulted in an immediate drop in arterial PO2 by approximately 7 torr, an increase in PCO2 by approximately 9 torr, and a small but significant increase in lactate levels. Cerebral oxidative metabolism was well maintained but required an increase in fractional oxygen extraction because the variable change in cerebral blood flow was insufficient to maintain oxygen delivery. A redistribution of upper body blood flow was evident, with that to the bran and heart variably maintained or increased whereas that to muscle tissue was markedly decreased. Repetitive umbilical cord occlusion over 1 hour resulted in a significant drop in fetal arterial pH, with the acidemia mixed as PCO2 increased approximately 6 torr, whereas lactate levels increased almost fourfold.
Although cerebral oxidative metabolism appears to be well maintained during moderate to severe variable-type fetal heart rate decelerations with umbilical cord occlusion, the need to increase fractional oxygen extraction and the redistribution of blood flow from carcass tissues may contribute to an accumulation of lactic acid both within the brain and systemically when such an insult occurs repeatedly.
American Journal of Obstetrics and Gynecology 11/1996; 175(4 Pt 1):929-36. · 3.47 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: To test the hypothesis that long-term hypoxemia causes premature activation of the fetal pituitary-adrenal function, we embolized the fetal side of the placenta in pregnant sheep and examined the changes in concentrations of immunoreactive adrenocorticotropic hormone (irACTH), cortisol, and prostaglandin E2 (PGE2) in fetal plasma, and levels and localization of proopiomelanocortin (POMC) mRNA in the pars distalis and the pars intermedia of the fetal pituitary. Twelve fetal sheep were studied (6 embolized and 6 control) for 21 days between 0.74 and 0.88 of gestation. Daily injections of nonradiolabeled microspheres were given into the fetal abdominal aorta to decrease fetal arterial oxygen content by 40-50% of the preembolization values. In the embolized group, concentrations of irACTH, PGE2, and cortisol in fetal plasma increased gradually and were significantly (P < 0.05) elevated above those of controls after day 10, day 16, and day 20, respectively. POMC mRNA levels in the pars distalis of the fetal pituitary were not different from those of controls but were significantly reduced in the pars intermedia (P < 0.05). We conclude that levels of POMC mRNA in the pars distalis are unchanged during long-term hypoxemia possibly because of negative feedback effects of elevated cortisol on the pituitary gland. During long-term fetal hypoxemia, there is a differential regulation of POMC mRNA expression in the pars distalis and pars intermedia.
The American journal of physiology 10/1996; 271(4 Pt 1):E678-85.
-
[show abstract]
[hide abstract]
ABSTRACT: Our goal was to determine the effect of chronic and acute umbilical-placental embolization on placental hemodynamic and fetal heart rate patterns in relation to fetal oxygenation in the near-term ovine fetus.
Daily fetal placental embolization was performed during 10 days in 9 sheep fetuses until fetal arterial oxygen content decreased by approximately 30%. Nine control fetuses received saline solution. Mean and pulsatile umbilical blood flow, perfusion pressure, placental vascular resistance, fundamental impedance, pressure pulsatility index, and umbilical artery resistance index corrected to a fetal heart rate of 160 beats/min were measured. On day 10 both groups were acutely embolized until fetal arterial pH decreased to approximately 7.00. Fetal heart rate was measured with the Sonicaid System 8000 (Oxford Sonicaid, Oxford, United Kingdom).
Chronic fetal placental embolization was associated with a progressive reduction in umbilical blood flow (p < 0.00001) and fetal arterial oxygen content (p < 0.001) whereas fetal heart rate patterns remained unaltered. A chronic increase in umbilical artery resistance index corrected to a fetal heart rate of 160 beats/min could be entirely explained only if the changes in umbilical artery pressure pulsatility index and the fundamental impedance were taken into account, in addition to the changes observed in placental vascular resistance. During acute embolization leading to a 50% reduction in umbilical blood flow (p < 0.0002) and a three times increase in placental vascular resistance (p < 0.0001), the most consistent change in fetal heart rate patterns related to progressive metabolic acidosis was an 84% decrease in absolute acceleration frequency (p < 0.0001) whereas short-term fetal heart rate variability remained unaltered.
Changes in umbilical artery resistance index induced by chronic umbilical-placental embolization resulting in fetal hypoxemia occurred before any changes in fetal heart rate patterns were detectable. A decrease in the absolute acceleration frequency was the only component of fetal heart rate patterns related to progressive metabolic acidosis in the near-term ovine fetus.
American Journal of Obstetrics and Gynecology 08/1996; 175(1):63-72. · 3.47 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: The purpose of this study was to examine the effect of chronic fetal placental embolization on fetal plasma prostaglandin E2 concentrations.
Fourteen pregnant sheep were studied (seven embolized and seven controls) for 10 days between 0.84 and 0.91 of gestation. Daily injections of nonradioactive microspheres were made to decrease fetal arterial oxygen content by 30% to 35% of preembolization values.
In response to repeated embolization, fetal plasma prostaglandin E2 concentrations increased significantly on day 1, declined to near control levels on days 2 to 6, but were significantly elevated again after day 7. Maternal prostaglandin E2 levels remained unchanged throughout the study. Fetal plasma prostaglandin E2 levels increased significantly with decreasing fetal oxygenation when fetal arterial oxygen content was < 2.0 mmol/L.
We conclude that there is increased production of prostaglandin E2 by the placenta during progressive fetal hypoxemia induced by fetal placental embolization. We speculate that the progressive increase in prostaglandin E2 may be an important hormonal adaptive mechanism to maintain fetal homeostasis during the development of placental insufficiency.
American Journal of Obstetrics and Gynecology 08/1995; 173(1):30-5. · 3.47 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Fetal growth and development are closely related to normal placental growth and function. We performed a study to determine the effect of a 10-day period of fetal hypoxemia induced by umbilical-placental hypoperfusion on tissue deoxyribonucleic acid synthesis rates in the 0.84 to 0.91 of gestation ovine fetus and placenta.
Daily fetal placental embolization was performed in four chronically catheterized sheep fetuses until fetal arterial oxygen content decreased by approximately 30% compared with preembolization values. Five control fetuses received vehicle only. On experimental day 10, the deoxyribonucleic acid synthesis rate was determined by injecting tritiated thymidine (1 mCi/kg) intravenously approximately 8 hours before the end of the study.
Fetal arterial oxygen decreased from 3.2 +/- 0.1 (SEM) mmol/L preembolization to 2.2 +/- 0.2 mmol/L on day 10 (p < 0.001) and remained unchanged in controls. On day 10 deoxyribonucleic acid synthesis rates were significantly reduced in embolized fetuses compared with controls, by 38% in cotyledons (83.0 +/- 15.1 vs 133.7 +/- 9.9 disintegrations/min/micrograms deoxyribonucleic acid, p < 0.05), 28% in the left ventricular wall (36.8 +/- 3.7 vs 51.0 +/- 4.7 disintegrations/min/micrograms deoxyribonucleic acid, p < 0.05), and 45% in the quadriceps muscle (15.4 +/- 4.0 vs 28.1 +/- 3.0 disintegrations/min/micrograms deoxyribonucleic acid, p < 0.05). Tritiated thymidine autoradiography demonstrated that cotyledonary deoxyribonucleic acid synthesis occurred exclusively in the fetal trophoblasts cells.
We concluded that a reduction in cotyledonary, quadriceps muscle, and left ventricular myocardium deoxyribonucleic acid synthesis rates are the earliest adaptive mechanisms of fetal growth associated with development of umbilical-placental insufficiency. We speculate that alteration in the myocardial deoxyribonucleic acid synthesis rate could be a major contributing factor in the deterioration of fetal myocardial function associated with increased placental vascular resistance.
American Journal of Obstetrics and Gynecology 06/1995; 172(5):1451-8. · 3.47 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: We report two cases for which computer interpretation of nonstress test indicated a flat decelerative trace in spite of normal fetal heart rate variability. Fetal behavioral state in the first case and signal loss in the second case were possibly responsible for this computerized interpretation of the tracings in the absence of fetal distress.
American Journal of Obstetrics and Gynecology 12/1994; 171(5):1379-81. · 3.47 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: The purpose of this study was to examine the effect of chronic fetal placental embolization on the fetal corticotropin, cortisol, and catecholamines concentrations and on myometrial contractility pattern.
Fourteen fetal sheep were studied (seven embolized, seven controls) for 10 days between 0.84 and 0.91 of gestation. Daily injections of nonradioactive microspheres were performed to decrease fetal arterial oxygen content by 30% to 35% of the preembolization value. Umbilical artery Doppler flow velocity waveforms were measured daily.
Chronic fetal placental embolization produced progressive fetal hypoxemia (p < 0.001) with changes in umbilical artery Doppler flow velocity waveforms indicative of a 25% increase in placental vascular resistance (p < 0.01). In response to chronic fetal hypoxemia there was a progressive increase in baseline fetal plasma norepinephrine concentration (p < 0.001). There was a transient fourfold to fivefold increase in baseline fetal plasma cortisol levels concomitant with a significant decrease in baseline immunoreactive corticotropin between days 7 and 9 of embolization (both p < 0.05), with a return to control values by day 10. There was a 57% increase in myometrial contracture frequency in the embolized group when compared with controls (p = 0.001).
During repetitive chronic placental damage that led to fetal hypoxemia, the fetal endocrine environment changed with time in a direction that would prevent the onset of premature activation of the hypothalamic-pituitary-adrenal axis and premature delivery.
American Journal of Obstetrics and Gynecology 03/1994; 170(3):929-38. · 3.47 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Waldenström hypergammaglobulinemic purpura is characterized by hypergammaglobulinemia, recurring purpura, and an elevated erythrocyte sedimentation rate. It is a rare disease and, to our knowledge, there have been no previous reports of its presence during pregnancy. We report a patient with this disease whose pregnancy was complicated by severe fetal growth restriction (FGR) and acute fetal distress.
A 24-year-old primigravid woman with a history of Waldenström hypergammaglobulinemic purpura and renal insufficiency developed FGR at 32 weeks' gestation. Cesarean delivery was performed at 33.5 weeks because of acute fetal distress, and a 1305-g male infant was delivered. Neonatal outcome was successful. No deterioration of the woman's medical condition occurred during or after her pregnancy.
Successful pregnancy outcome is possible in women with Waldenström hypergammaglobulinemic purpura. In view of the risk of FGR, close monitoring of fetal growth and well-being is recommended in women with this condition.
Obstetrics and Gynecology 11/1993; 82(4 Pt 2 Suppl):685-7. · 4.73 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Background: Waldenstrom hypergammaglobulinemic purpura is characterized by hypergammaglobulinemia, recurring purpura, and an elevated erythrocyte sedimentation rate. It is a rare disease and, to our knowledge, there have been no previous reports of its presence during pregnancy. We report a patient with this disease whose pregnancy was complicated by severe fetal growth restriction (FGR) and acute fetal distress.
Case: A 24-year-old primigravid woman with a history of Waldenstrom hypergammaglobulinemic purpura and renal insufficiency developed FGR at 32 weeks' gestation. Cesarean delivery was performed at 33.5 weeks because of acute fetal distress, and a 1305-g male infant was delivered. Neonatal outcome was successful. No deterioration of the woman's medical condition occurred during or after her pregnancy.
Conclusion: Successful pregnancy outcome is possible in women with Waldenstrom hypergammaglobulinemic purpura. In view of the risk of FGR, close monitoring of fetal growth and well-being is recommended in women with this condition. (Obstet Gynecol 1993;82:685-7)
(C) 1993 The American College of Obstetricians and Gynecologists
Obstetrics and Gynecology 09/1993; 82(4). · 4.73 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: This study was designed to determine the intraobserver and interobserver variability in the visual assessment of fetal heart rate tracings and to evaluate the accuracy of the visual detection of accelerations and decelerations when compared with computerized fetal heart rate analysis.
One hundred antepartum fetal heart rate tracings, of good quality and of 30 minutes' duration, were visually assessed by five expert observers on three occasions during a 12-month period. There were a total of seven questions related to either judgment or accuracy of each recording. Visual detection of fetal heart rate acceleration, deceleration, and estimated baseline was compared with computerized analysis. Statistical significance was determined by kappa coefficient and contingency table chi 2 analysis.
Analysis with kappa coefficient reflecting intraobserver and interobserver agreement of judgment-related questions indicated poor agreement between observers when assessing short-term fetal heart rate variability (kappa 0.18), when making a decision to stop or continue recording (kappa 0.39), and when judging whether there is concern regarding fetal heart rate tracing (kappa 0.26). When compared with computerized analysis, clinicians had a tendency to recognize tracings as normal. In particular, they failed to identify 35% of tracings with 0 or 1 acceleration and failed to detect 92% of fetal heart rate decelerations. Variable decelerations associated with fetal movements were the major source of disagreement between observers and the computer. Only the estimation of baseline fetal heart rate had a high level of accuracy.
We concluded that the poor level of accuracy in several components of the nonstress test was responsible for the low interobserver agreement seen in simple judgment-related questions such as decision to continue or stop fetal heart rate recordings.
American Journal of Obstetrics and Gynecology 04/1993; 168(3 Pt 1):842-7. · 3.47 Impact Factor
