1,721,003 research outputs found
Longitudinal study of umbilical and portal venous blood flow to the fetal liver: low pregnancy weight gain is associated with preferential supply to the fetal left liver lobe
No full textRecent data suggest that umbilical venous perfusion of the fetal liver has an important influence on fetal growth and postnatal liver function, and that maternal factors in late pregnancy modify this circulation. In a longitudinal study of 160 low-risk pregnancies, we determined how umbilical and portal venous blood flows to the fetal liver changed during gestation, and examined the hypothesis that maternal body mass index and pregnancy weight gain influenced fetal liver blood flows. We measured blood flows in the umbilical and portal veins, left portal branch, and ductus venosus using ultrasound. Normalizing for estimated fetal weight, fetal liver total venous blood flow fell from 84 to 57 mL. min(-1). kg(-1) during 21-39 wk of gestation; toward term the portal contribution increased (from 14 to 20%) and the umbilical contribution fell, whereas distribution between the left and right liver lobes was stable, 60%/40%. Greater flow of nutrient-rich umbilical venous blood to the liver was associated with higher birth weight and neonatal ponderal index. Maternal body mass index was not related to fetal liver blood flows, but low pregnancy weight gain strongly influenced flow distribution between the right and left liver lobes, sparing the left lobe and increasing the difference between lobes by 16%
Altered development of fetal liver perfusion in pregnancies with pregestational diabetes
No full text
Background Pregestational diabetes is associated with fetal macrosomia, and umbilical perfusion of the fetal liver has a role in regulating fetal growth. We therefore hypothesized that pregestational diabetes alters fetal liver blood flow depending on degree of glycemic control. Methods In a prospective study, 49 women with pregestational diabetes underwent monthly ultrasound examinations during 24-36 gestational weeks. Blood flow was determined in the umbilical vein, ductus venosus and portal vein, and blood velocity was measured in the left portal vein, the latter reflecting the watershed between splanchnic and umbilical flow. The measurements were compared with reference values by z-score statistics, and the effect of HbA
1c
assessed. Results The umbilical venous flow to the liver (z-score 0.36, p = 0.002), total venous liver flow (z-score 0.51, p<0.001) and left portal vein blood velocity (z-score 0.64, p<0.001), were higher in the study group. Normalized portal venous flow was lower (z-score -0.42, p = 0.002), and normalized total venous liver flow tended to be lower after 30 gestational weeks (z-score -0.54, p = 0.047) in the diabetic pregnancies compared with reference values from a low-risk population. The left portal vein blood velocity was positively, and the portal fraction of total venous liver flow negatively correlated with first trimester HbA
1C
. Conclusions In spite of increased umbilical blood distribution to the fetal liver, graded according to glycemic control, the total venous liver flow did not match third trimester fetal growth in pregnancies with pregestational diabetes, thus contributing towards increased perinatal risks and possibly altered liver function with long-term metabolic consequences.
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Fetal growth restriction is associated with prioritization of umbilical blood flow to left hepatic lobe, at the expense of the right lobe
No full textEighty to 85% of the venous perfusion to the fetal liver is from the umbilical vein, the rest from the portal vein. Umbilical venous flow to the liver is essential for intrauterine growth, and is impaired in placental insufficiency. We hypothesized that in growth-restricted fetuses portal blood flow compensates for insufficient umbilical blood flow to the liver. In 29 fetuses with fetal growth restriction (estimated fetal weight < or =5th percentile), we used ultrasound to measure blood flows in the umbilical vein, ductus venosus, left portal vein, and main portal stem. Compared with normal fetuses, both absolute and normalized total venous liver blood flows were reduced in growth-restricted fetuses, related to the degree of placental compromise and equally affecting both liver lobes. However, portal replaced umbilical flow to the right lobe, in a manner graded according to placental vascular resistance; in extreme cases, the right lobe received no umbilical perfusion. In fetal growth restriction, the liver suffers from venous hypoperfusion, and portal blood partially replaces umbilical flow to the right lobe; this will result in right liver lobe hypoxemia. This striking prioritization in nutrient delivery of left over right lobes suggests an adaptive response to poor placental perfusion that may have functional consequence
Optimal fetal growth – a misconception?
No full textAlterations in fetal growth trajectory, either in terms of individual organs or the fetal body, constitute part of a suite of adaptive responses that the fetus can make to a developmental challenge such as inadequate nutrition. Nonetheless, despite substantial changes in nutrition in many countries over recent centuries, mean birthweight has changed relatively little. Low birthweight is recognised as a risk factor for later noncommunicable disease, although the developmental origins of such risk are graded across the full range of fetal growth and birthweight. Many parental and environmental factors, some biological, some cultural, can influence fetal growth, and these should not be viewed as abnormal. We argue that the suggestion of establishing a universal standard for optimal fetal growth ignores the breadth of these normal fetal responses. It may influence practice adversely, through incorrect estimation of gestational age and unnecessary elective deliveries. It raises ethical as well as practical issues
Fetal superior mesenteric artery: longitudinal reference ranges and evidence of regulatory link to portal liver circulation
No full textObjective: To establish longitudinal reference ranges for the fetal superior mesenteric artery (SMA) flow
velocity and pulsatility index (PISMA). Also to examine the hemodynamic relationship to venous liver
perfusion and umbilical flow distribution in the liver, to other splanchnic arteries, and more generally to the
middle cerebral and umbilical artery.
Methods: Prospective longitudinal study of 161 low-risk pregnancies using Doppler recordings including the
SMA, repeated on 3–5 occasions at 3–5 weekly intervals. Umbilical venous flow was estimated, blood velocity
in the shunt ductus venosus represented umbilico-caval (i.e. porto-caval) pressure gradient, and left portal
vein blood velocity represented umbilical distribution within the liver. The correlation between PISMA and the
splenic and hepatic artery PI were analysed (PISA and PIHA), and the association to middle cerebral and
umbilical artery PI (PIMCA and PIUA) assessed.
Results: Reference ranges for the SMA for gestational weeks 21–39 were based on 589 observations. Low
impedance in the SMA (i.e. low PISMA) was associated with low umbilical flow and porto-caval pressure
gradient (i.e. b10th centile), and high distribution of umbilical flow to the right lobe (i.e. left portal vein blood
velocity N90th centile). PISMA correlated weakly with PISA and PIHA (r=0.30, 95%CI 0.22–0.37, and r=0.39, 95%
CI 0.27–0.51, respectively). PISMA was positively associated with PIMCA and PIUA.
Conclusion: We have provided longitudinal reference ranges for fetal SMA flow velocity and PI, and shown
that the SMA, which perfuses the fetal gut, is also involved in the regulation of the liver perfusion
Fetal liver-sparing cardiovascular adaptations linked to mother's slimness and diet
No full textFetal adaptations to impaired maternoplacental nutrient supply include altered regional blood flow. Whether such responses operate within the normal range of maternal body composition or diet is unknown, but any change in fetal liver perfusion could alter hepatic development, with long-term consequences for the risk of cardiovascular and metabolic disease. In 381 low-risk pregnancies, we found that the fetuses of slimmer mothers with lower body fat stores and those eating an unbalanced diet had greater liver blood flow and shunted less blood away from the liver through the ductus venosus at 36 weeks gestation. Consequences of such "liver-sparing" may underlie the increased cardiovascular risk of people whose mothers were slimmer and had lower body fat stores in pregnancy
Hepatic artery hemodynamics suggest operation of a buffer response in the human fetus
Full text linkAfter birth, the hepatic artery buffer response helps to maintain liver perfusion. Here, the authors establish a Doppler technique to measure fetal hepatic artery flow velocity and test the hypothesis that the buffer response also operates prenatally. Women with low-risk pregnancies were recruited to a longitudinal study (N = 161). Measurement techniques and reference ranges for hepatic artery velocities and pulsatility index (PI) were established. Ductus venosus peak velocity (VDVps) represented the portocaval pressure gradient, and umbilical venous flow (QUV) represented portal flow. Reference ranges were established for the more accessible left hepatic artery branch. Hepatic artery PI was lower in fetuses with VDVps <10th centile (P < .05) and in those with QUV <10th centile ( P < .0001). Conversely, hepatic artery PI was higher in those with QUV >90th centile (P < .0001). The authors establish a method for measuring fetal hepatic arterial blood velocity, provide reference ranges, and show that the hepatic artery buffer response operates prenatally
Circulatory responses to maternal hyperoxaemia and hypoxaemia assessed non-invasively in fetal sheep at 0.3-0.5 gestation in acute experiments
No full textObjectives: to determine fetal haemodynamic responses to hyperoxaemia and hypoxaemia in early pregnancy.Design: repeated measurements in acute experiments.Setting: experimental physiology laboratory.Methods: non-invasive Doppler ultrasound of the umbilical vein, ductus venosus, umbilical and common carotid arteries of 12 fetal lambs (0.27–0.56 gestation) during maternal hyperoxaemia and hypoxaemia under ketamine anaesthesia. The effect of gestational age, hyperoxaemia, and hypoxaemia were assessed based on analysis of variance for dependent measurements and P? 0.05 was considered significant. Differences between groups were considered significant if the 95% confidence interval did not include zero.Results: gestational age had a significant effect on the blood velocity in the umbilical vein and ductus venosus. There were no circulatory changes during hyperoxaemia, but a simultaneous increase of pCO2 was an important confounder. However, hypoxaemia caused significantly reduced heart rate, reduced maximum and weighted mean blood velocity, and augmented pulsation in the umbilical vein. Hypoxaemia also caused reduced velocities in the ductus venosus (peak velocity during systole and minimum during diastole, and time-averaged velocity) and augmented pulsation of the flow velocity. Additionally, the pulsatility of blood flow increased in the umbilical artery and was reduced in the common carotid artery.Conclusions: maternal hypoxaemia in early pregnancy causes similar fetal circulatory responses to those in late pregnancy: bradycardia, reduced venous flow velocities, augmented pulsatility in veins and a redistributional flow velocity pattern of the umbilical and common carotid arteries
Redistribution pattern of fetal liver circulation in intrauterine growth restriction
No full textObjectiveFetal liver blood supply is an important determinant of fetal growth and adaptation. Most fetal liver blood supply is from the umbilical vein, but the portal vein contributes 14-20% and studies of low-risk pregnancies suggest the splanchnic arteries are also involved in the homeostasis of fetal liver perfusion. Here we determine the circulatory pattern of the fetal liver in intrauterine growth restriction (IUGR). Design. Cross-sectional study. Population. Thirty-one IUGR fetuses (estimated fetal weight <5th centile). Methods Pulsatility index (PI) measurements of the umbilical, middle cerebral, splenic, hepatic, and superior mesenteric arteries were compared with a reference population and related to umbilical venous flow, umbilico-caval pressure gradient (assessed by ductus venosus peak velocity) and venous distribution within the liver (assessed by flow velocity in the left portal vein). ResultsThirteen of 31 IUGR fetuses had umbilical artery PI > 97.5 centile and 13 showed a middle cerebral artery brain-sparing pattern (PI Z-score < - 2). In IUGR, umbilical venous flow was lower and less umbilical blood was distributed to the right liver lobe, while the umbilico-caval pressure gradient was kept normal. The hepatic and splenic arteries, but not the superior mesenteric artery, had low PI compared with the reference population. ConclusionsIUGR fetuses with increased or normal umbilical artery PI maintained venous perfusion pressure to the liver while distributing less umbilical blood to the right liver lobe. They showed regional splanchnic arterial redistribution with low splenic and hepatic artery PI, implying increased portal venous flow and direct arterial contribution to hepatic perfusion, respectively
Functional ultrasound of the anal canal. The effect of pregnancy and childbirth
Full text linkThis thesis is concerned with functional three-dimensional ultrasound of the anal canal. Comparing acquisitions assessed with endoanal- and transvaginal transducers, the transvaginal transducer turned out to be as good as the endovaginal transducer. In addition, the curvatures, position and dimensions of the undisturbed anatomical structures in the anal canal, including the anal mucosa, could be described using the transvaginal acquisitions. The transvaginal technique provided information of how the curvatures, positions and dimensions changed during voluntary squeeze of the pelvic floor. The anal mucosa constitutes 40 % of the structures in the anal canal. Voluntary squeeze caused a distorted mucosa at the ano-rectal junction, increased bowel bend, an increased angle between the anal canal and vagina, and elongation of the canal. These observations could not be studied in acquisitions assessed with the endoanal transducer, which straightened and moved the anal mucosa away during application. Pregnancy affects anal continence, but the natural development of the anal canal during pregnancy and childbirth is not known. The impact of pregnancy was an elongation of the canal and a 20% increase in volume of the anal sphincters and anal mucosa. Much of the effects of voluntary squeeze were maintained
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