Kilogram Of Fetal Weight Research Articles

The Fetal Liver Afferent Venous Flow Volumes in Fetuses With Appropriate for Gestational Age Birth Weight.

The present study aimed: 1) to simultaneously investigate the relationship between blood flow volumes of the two fetal liver afferent venous systems of normally appropriate for gestational age newborns. 2) to establish the normal reference range centiles values that will serve as a basis for future investigations. A cross-sectional, prospective study of singleton low obstetric risk pregnancies. Doppler examination included the measurement of the umbilical and the main portal vein vessels' diameters and time-averaged maximum velocity. The absolute and per kilogram of estimated fetal weight flow volumes and the ratio between the placental and portal blood volume flow were calculated from these data. Three hundred and sixty-three pregnant women were included in the study. The umbilical and portal flow volumes' capacity to provide blood flow per kilogram of fetal weight, in the period of maximum fetal growth, was diverse. The placental flow decreased continuously from a mean of 121.2 mL/min/kg at the 20th week of gestation to 64.1 mL/min/kg at the 38th week of gestation. Meanwhile, the portal flow volume per kilogram of fetal weight increased from 9.6 mL/min/kg at 32 weeks of gestation to 10.3 at the 38th week of gestation. This resulted in a decrease in the umbilical to portal flow volume ratio from 13.3 to 9.6 during this period. Our results indicate that in the period of maximum fetal growth, the placental/portal ratio diminishes emphasizing the portal flow's predominance with low oxygen and nutrient supply to the liver.

Thyroid hormone is required for growth adaptation to pressure load in the ovine fetal heart

Thyroid hormone exerts broad effects on the adult heart, but little is known regarding the role of thyroid hormone in the regulation of cardiac growth early in development and in response to pathophysiological conditions. To address this issue, we determined the effects of fetal thyroidectomy on cardiac growth and growth-related gene expression in control and pulmonary-artery-banded fetal sheep. Fetal thyroidectomy (THX) and/or placement of a restrictive pulmonary artery band (PAB) were performed at 126 ± 1 days of gestation (term, 145 days). Four groups of animals [n = 5-6 in each group; (i) control; (ii) fetal THX; (iii) fetal PAB; and (iv) fetal PAB + THX] were monitored for 1 week prior to being killed. Fetal heart rate was significantly lower in the two THX groups compared with the non-THX groups, while mean arterial blood pressure was similar among groups. Combined left and right ventricle free wall + septum weight, expressed per kilogram of fetal weight, was significantly increased in PAB (6.27 ± 0.85 g kg(-1)) compared with control animals (4.72 ± 0.12 g kg(-1)). Thyroidectomy significantly attenuated the increase in cardiac mass associated with PAB (4.94 ± 0.13 g kg(-1)), while THX alone had no detectable effect on heart mass (4.95 ± 0.27 g kg(-1)). The percentage of binucleated cardiomyocytes was significantly decreased in THX and PAB +THX groups (∼16%) compared with the non-THX groups (∼27%). No differences in levels of activated Akt, extracellular signal-regulated kinase or c-Jun N-terminal kinase were detected among the groups. Markers of cellular proliferation but not apoptosis or expression of growth-related genes were lower in the THX and THX+ PAB groups relative to thyroid-intact animals. These findings suggest that in the late-gestation fetal heart, thyroid hormone has important cellular growth functions in both physiological and pathophysiological states. Specifically, thyroid hormone is required for adaptive fetal cardiac growth in response to pressure overload.

Endothelin 1 and leptin in the pathophysiology of intrauterine growth restriction

Objectives: To evaluate the relationship of endothelin 1 (ET-1) and leptin concentrations in women and newborns following a pregnancy complicated with intrauterine growth restriction (IUGR). Methods: Twenty-five women with a pregnancy complicated with IUGR at 19 different gestational ages were matched with women with uncomplicated pregnancies. Blood samples from the umbilical artery and maternal peripheral venous circulation were collected at delivery, and ET-1 and leptin levels were determined from the blood samples. Data relating to obstetric complications (e.g., pregnancy-induced hypertension), delivery (e.g. mode, birth weight, signs of intrapartum fetal distress, and Apgar scores) were also recorded. Results: Mean maternal ET-1 (13.4±6.2–9.9±2.9 pmol/l) and mean fetal ET-1 (14.5±4.2–11.7±3.1 pmol/l) concentrations were significantly higher when women had experienced pregnancies complicated with IUGR than when they had had normal pregnancies. Mean fetal leptin concentration was significantly lower in the study group (6.8±2.2 ng/ml) than in the control group (10.6±3.6 ng/ml ( P<0.05). However, fetal leptin per kilogram of fetal weight was not significantly different in the study group (3.16±1.18 ng/ml) than in the control group (3.23±0.96 ng/ml) ( P>0.05, paired t-test). However, a statistically significant correlation was observed between fetal leptin concentrations per kilogram of fetal weight and fetal endothelin concentrations in pregnancies complicated with IUGR ( r=0.546; P<0.05). Conclusions: These results suggest the intertwined roles of ET-1 and leptin in the pathophysiology of IUGR. Further studies concerning interaction between these peptides in different pregnancy conditions may provide important information about the actions of ET-1 and leptin on fetal growth.

A longitudinal study of quantitative uterine blood flow with the use of color power angiography in appropriate for gestational age pregnancies

Objective: The purpose of this study was to examine longitudinally changes in quantified blood volume flow in the uterine arteries during pregnancy with the use of color power angiography. Study Design: Color power angiography was used to quantify volume flow in the uterine arteries of 57 women with singleton uncomplicated pregnancies between 20 and 38 weeks’ gestation. Comparisons were made between blood flow in the 2 arteries in relation to the location of the placenta. Linear regression models were used to estimate gestational age derived volumetric changes in these vessels. Results: The diameter of the uterine arteries increased from 2.6 mm (SD, 0.2 mm) at 20 weeks to 4.8 mm (SD, 0.7 mm) at 38 weeks of gestation. The total uterine artery blood volume flow increased from 513 mL/min (SD, 127 mL/min) at 20 weeks to 970 mL/min (SD, 193 mL/min) at 38 weeks. The rate of increase was maximum between 20 and 24 weeks (39 mL/min per week). The laterality of the placenta significantly affected the diameter and blood volume flow in each uterine artery. The diameters on the ipsilateral side were significantly greater (by 10.8% ± 2.4%) than the diameters on the contralateral side at all gestations (P <.05). Similarly, blood volume flow was significantly greater (by 17.8% ± 2.2%) on the ipsilateral side at all gestations (P <.05). There were, however, no statistically significant differences between the vessel diameters and blood volume flow in those cases in which the placenta was central. Total uterine artery volume flow per kilogram of estimated fetal weight decreased from 1544 mL/kg per minute at 20 weeks to 296 mL/kg per minute at 38 weeks of gestation. Conclusion: Total quantified uterine artery blood volume flow increases while blood flow per kilogram of fetal weight decreases with gestation. Blood volume flow in the ipsilateral artery to the placenta was significantly higher than that in the contralateral artery. Calculating total uterine artery volume flow by doubling the blood flow from 1 artery (as was previously done) may therefore either result in an over or underestimation, depending on the relationship between the vessel and the laterality of the placenta. Color power angiography is a simple noninvasive tool for determining uterine artery blood volume flow. (Am J Obstet Gynecol 2001;185:608-13.)

Relationship of umbilical vein blood flow to growth parameters in the human fetus

Objective: Our purposes were to determine the relationship of the growth of umbilical blood flow to growth in body measurements of human fetuses in uncomplicated pregnancies. The study also aimed to assess the relative contributions of growth in umbilical vein diameter and of increased velocity to the increase in umbilical blood flow. Study Design: An animal study was conducted to assess the accuracy of umbilical vein blood flow measurements obtained by triplex mode ultrasonography. Seven pregnant ewes underwent triplex mode umbilical vein flow determination. These results were compared with historical flow data obtained by a steady-state diffusion technique in 34 ewes matched for gestational age and weight. In a separate study performed on human beings, reproducibility and precision of triplex mode flow determination were assessed, as were the relationships between umbilical vein flow and gestational age and head and abdominal circumferences. This cross-sectional study was performed with 70 healthy fetuses ranging from 20 weeks’ gestation to term. Best-fit interpolating equations and confidence limits were calculated for blood flow measurements versus gestational age and head and abdominal circumferences. Results: In the validation study performed on sheep there were no significant differences between triplex mode and steady-state measurement groups with respect to gestational age or weight. The umbilical vein flows were similar between triplex mode and steady-state measurement groups ( P = .881). In the human study the intraobserver and interobserver coefficients of variation for the vein diameter, mean velocity, and absolute umbilical vein blood flow varied from 2.9% to 12.7%. The mean duration of examination was 3 ± 1 minutes. The umbilical vein diameter and mean velocity increased throughout pregnancy. The absolute umbilical vein flow increased exponentially from 97.3 mL/min at midgestation to 529.1 mL/min at 38 weeks’ gestation, whereas umbilical vein flow per kilogram of fetal weight did not change significantly with gestational age. There was a strong correlation between absolute umbilical vein flow and the fetal head and abdominal circumferences. Conclusions: The triplex mode ultrasonographic technique can play an innovative role in obtaining quick and reproducible measurements of umbilical vein blood flow. The approach was validated with a sheep model. Umbilical vein blood normalized for fetal weight (milliliters per minute per kilogram of fetal weight) and absolute flow (in milliliters per minute) are consistent with previous human studies. We have established new reference values of umbilical vein blood flow relative to head and abdominal circumferences. The growth of umbilical venous diameter accounted for most of the growth in umbilical vein flow. (Am J Obstet Gynecol 1999;181:174-9.)

The significance of high umbilical venous blood flow measurements in a high-risk population.

We report a statistical analysis of 893 high-risk patients who underwent Doppler sonographic estimation of umbilical venous blood flow within 2 weeks of delivery. Patients with red cell isoimmunization were excluded. In a total of 84 patients, the umbilical venous flow rate was above the 95th centile for normal pregnancy. This finding was associated significantly with an increased prevalence of maternal diabetes mellitus, polyhydramnios, fetal abnormalities, premature delivery, low 5 min Apgar scores, and neonatal death. Umbilical venous flow rates per kilogram of fetal weight above the 95th centile were recorded in 93 patients. This finding was associated significantly with an increased rate of antepartum hemorrhage, premature delivery, low 5 min Apgar scores, longer stays in intensive care nursery, and neonatal death. Low umbilical venous blood flow rates have been investigated extensively and associated with impaired perinatal outcome. The work reported in this paper indicates that a percentage of fetuses will have abnormally high umbilical venous flow rates and that this is also indicative of increased risk.

Venous and hepatic vascular responses to indomethacin and prostaglandin E 1 in the fetal lamb

Evidence is accumulating that prostaglandins affect the tone of the ductus venosus. Therefore prostaglandins might alter the distribution of umbilical venous return between the ductus venosus and liver. We have examined the effect of indomethacin and prostaglandin E1 on the vascular resistance of the umbilical-placental circulation, ductus venosus, and liver in 14 chronically instrumented fetal lambs. We found that indomethacin caused a nearly twofold increase in the vascular resistance of both the ductus venosus and liver. Prostaglandin E1, administered 70 minutes after indomethacin at a dose of 0.41 +/- 0.09 (SEM) micrograms/min per kilogram of fetal weight, decreased umbilical-placental blood flow, increased the vascular resistance of the umbilical arteries and placenta, and reversed the elevation of the vascular resistances of the ductus venosus and liver. Because both indomethacin and prostaglandin E1 affected the resistances of the ductus venosus and liver to the same extent, it is unlikely that prostaglandins of the E series mediate the change in distribution of umbilical venous return between the ductus venosus and liver during fetal stress.

Norepinephrine elevation in the fetal lamb: oxygen consumption and cardiac output

In an effort to determine if placental diffusion reserves exceed fetal O2 requirements, we increased fetal O2 consumption (VO2) by infusing 1.7-11.5 microgram of norepinephrine (NE) . min-1. After 50 min of infusion VO2 rose 25% to 10.2 from 8.2 ml . min-1 . kg fetal wt-1. Placental CO diffusing capacity remained essentially unchanged from control, 0.49 +/- 0.05 (SE) ml . min-1. Torr-1 . kg-1, During the first 5 min of NE infusion fetal arterial blood pressure increased 29%, while heart rate decreased 15%. In addition, coronary, pulmonary, and umbilical blood flow, expressed per kilogram of fetal weight as determined by use of labeled microspheres, increased 50, 162, and 25%, respectively (P less than 0.05), although fetal cardiac output remained constant at 538 +/- 23 (SE) ml . min-1 . kg-1. Finally, we determined the NE-blood pressure dose-response relations for the fetus; Blood pressure increased with doses up to 1 microgram . min-1 . kg-1, but failed to rise further with higher doses. We conclude that 1) fetal VO2 increases with NE infusion 2) the placental reserve for O2 diffusion exceeds normal requirements, and 3) NE infusion is associated with increased blood pressure, bradycardia, and a redistribution of blood flows to the heart, lungs, and placenta despite a constant cardiac output.

Maturational changes in the fetal glomerular filtration rate

Few data are available documenting the evolution of glomerular filtration rate (GFR) during gestation. In order to investigate this aspect, 33 fetal sheep have been studied, with the use of an intrauterine fetal preparation. It appears that the actual GFR (AGFR) in milliliters per minute increased during the last third of gestation without a significant increase in CFR expressed as milliliters per minute per kilogram of fetal weight (GFR-FW) and as milliliters per minute per gram of kidney weight (GFR-KW). It is suggested that a parallel and constant increase in AGFR and in total fetal weight or kidney weight might explain the absence of variation in GFR-FW or GFR-KW during the last third of gestation.

Placental transfer of glutamate and its metabolites in the primate

When radioactive glutamate was infused into pregnant rhesus monkeys, 69 to 88 per cent of radioactivity in the maternal plasma remained in association with glutamate while 10 to 22 per cent was converted to glucose. In the fetal plasma, glucose and lactate accounted for more than 80 per cent of radioactivity, with less than 2 per cent of the label found in glutamate. Maternal glutamate infusions resulting in a ten- to twenty-fold increase in maternal plasma glutamate levels (60 to 100 μmoles per 100 ml.) had no effect upon fetal glutamate levels. Infusions producing maternal glutamate levels 70 times normal (280 μmoles per 100 ml.) did result in some transfer of glutamate to the fetal circulation. Labeled glutamate administered to the fetus at 1.5 to 2.4 Gm. per kilogram of fetal weight did not result in glutamate transfer to the maternal circulation. Infusion of glutamate to the fetus at 5 Gm. per kilogram of fetal weight increased fetal plasma glutamate levels to 2,000 μmoles per 100 ml. and resulted in some transfer of glutamate to maternal circulation. Glutamate metabolites (lactate and glucose) were readily transferred across the placenta in either direction. These studies indicate that the primate placenta is virtually impermeable to glutamate unless extreme elevations of plasma glutamate are induced.

Effects of lidocaine on heart rate, blood pressure, and electrocorticogram in fetal sheep

Effects of lidocaine on blood pressure, heart rate, electrocortical activity, pH, and blood gases were studied in chronically catheterized sheep fetuses in utero. Lidocaine infused at a constant rate of less than I mg. · min.−1 · Kg.−1 into a fetal femoral vein did not cause changes in fetal blood pressure, heart rate, pH, or blood gases. Infusion rates above 1 mg. · min.−1 · Kg.−1 caused sudden, phasic increases in blood pressure in the majority of the fetuses. The heart rate increased in association with each phasic increase in blood pressure. In some fetuses the heart rate decelerated after the initial acceleration. Fetal electrocortical recordings showed that each phasic change in blood pressure and heart rate was secondary to epileptiform activity. The concentration of lidocaine in fetal arterial blood was 11.6 ± 3.8 μg per milliliter when the first phasic increase in blood pressure occurred. Tracheal pressure recordings showed deep fetal breathing movements with each epileptiform activity. It is concluded that lidocaine causes convulsions in the fetal sheep and that the cardiovascular changes are due to central stimulation during these convulsions. In newborn lambs lidocaine produced similar epileptiform activity associated with tonic-clonic convulsions and cardiovascular changes. Fetal arterial pH was not affected until the phasic changes occurred, after which the pH fell rapidly in the majority of the fetuses. In three paralyzed fetuses the pH also decreased at the onset of phasic increases in blood pressure. This indicated that muscular activtiy was not the main cause of the acidemia during fetal epileptiform activity. Bolus injections of lidocaine in doses of 3.0 to 22.2 mg. per kilogram of fetal weight caused an immediate decrease in blood pressure and heart rate. These changes were related to the dose of lidocaine. The convulsive dose of lidocaine as a bolus injection ranged from 8.0 to 22.2 mg. per kilogram.

Some effects of meperidine hydrochloride on maternal and fetal sheep

Single intravenous injection into the pregnant ewe of meperidine HCl in dosages of 0.85 to 2.5 mg. per kilogram of maternal weight and 14.7 to 76.9 mg. per kilogram of fetal weight was not associated with significant effects on maternal and fetal arterial blood pressure and heart rate. Furthermore, no significant changes could be found in maternal arterial, fetal arterial, and umbilical venous blood gas values or acid-base values. The mean dosage of lidocaine HCl in milligrams per minute required for satisfactory continuous spinal anesthesia in the pretest period was 3.66 times that required following the injection of meperidine HCl.