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

Abstract

Recent 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 ⅐ min Ϫ1 ⅐ kg Ϫ1 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%. T he developmental origins of health and disease hypothesis established a link between an adverse intrauterine environment and cardiovascular disease in adult life (1,2). There is strong evidence from epidemiologic studies and animal experiments that an adverse intrauterine environment is associated with raised levels of cardiovascular risk factors controlled by the liver (3). The role of the fetal liver for intrauterine growth and development has therefore come into focus of research.In fetal sheep, experimental reduction in umbilical venous liver perfusion results in decreased synthesis of insulin-like growth factors by the fetal liver, decreasing the cellular proliferation rate in peripheral tissues and impairing fetal growth (4,5). In human fetuses, venous liver blood flow was shown to be modulated by maternal diet and body composition (6).The fetal liver receives venous blood from the umbilical and portal veins (PVs). The umbilical vein (UV) directs nutrient-rich placental blood predominantly to the left liver lobe, whereas nutrient-depleted blood from the PV is directed to the right liver lobe (7). This selective perfusion pattern is thought to be the main reason for differences in micro architecture (8), hematopoiesis (9) and gene and enzyme expression (10,11).Although single components of the venous liver circulation such as umbilical blood flow (12-14) and shunting through the ductus venosus (DV) (15,16) have been investigated earlier, little is known about the distributions of umbilical and portal blood flows in the human fetus.The aim of the present study was to study simultaneously the umbilical and portal venous circulations and the blood flow distribution to the liver lobes in the second half of ...

Human supraphysiological gestational weight gain and fetoplacental vascular dysfunction

“…34 Since the optimal diameter of vein rings from both groups was similar, the possibility of an altered modulation of umbilical vein tone rather than a tonic vasconstriction of these vessels is likely in spGWG. Indeed, a reduced response to insulin in vein rings from spGWG may not be due to an altered mechanical response of the vascular smooth muscle in the human fetoplacental vasculature since the response to the NO donor SNP was unaltered in these vessels.…”

Fetal Liver Blood Flow Distribution: Role in Human Developmental Strategy to Prioritize Fat Deposition versus Brain Development

“…Maternal low protein diets have also been shown to alter epigenetic processes in hepatocytes in the offspring [27], with permanent consequences including altered liver carbohydrate and fat metabolism [27] and a predisposition to adult obesity and reduced lifespan [26], [28]. Moreover, a reduction in liver glucocorticoid receptor and fibrinogen gene expression caused by a low protein maternal diet was confined to the left hepatic lobe [29]; in circumstances of high ductus venosus liver shunting there is differential perfusion of the right and left hepatic lobes, with preferential perfusion of the left hepatic lobe by umbilical blood [30].…”

“…DV TAMX was calculated as the mean during three heart cycles. Blood flow (Q) was calculated as Q = h·(D/2) 2 ·π·TAMX, where D = vessel diameter (mean of 5–10 measurements [37]) and h = spatial blood velocity profile coefficient (UV = 0.5; DV = 0.7) [30], [38]–[40]. Intra-class correlation coefficients (random-effects regression) to assess intra-observer variation were 0.97 and 0.96 for the UV and DV diameter, respectively.…”

Prospective association of fetal liver blood flow at 30 weeks gestation with newborn adiposity

“…Portal vein flow, however, accounts for only a small proportion of f LBF and is not believed to be a source of nutrient substrate from the placenta. 61 We used fetal abdominal circumference as a proxy measure of fetal liver volume. Direct measurement of fetal liver volume measurement with 3D ultrasonography 62 might add precision, and this represents a future research direction.…”