Ductus venosus shunting in the fetal venous circulation: regulatory mechanisms, diagnostic methods and medical importance.
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Ductus venosus shunting in the fetal venous circulation: regulatory mechanisms, diagnostic methods and medical importance. / Tchirikov, Mikhail; Schröder, H J; Hecher, Kurt.
in: ULTRASOUND OBST GYN, Jahrgang 27, Nr. 4, 4, 2006, S. 452-461.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Ductus venosus shunting in the fetal venous circulation: regulatory mechanisms, diagnostic methods and medical importance.
AU - Tchirikov, Mikhail
AU - Schröder, H J
AU - Hecher, Kurt
PY - 2006
Y1 - 2006
N2 - The fetal liver is located at the crossroads of the umbilical venous circulation. Anatomically, the ductus venosus (DV) and the intrahepatic branches of the portal vein are arranged in parallel. The actual DV shunting rate, i.e. the percentage of umbilical blood flow entering the DV measured by Doppler velocimetry, seems to be lower than that estimated using radioactively-labeled microspheres. In human fetuses the DV shunting rate is about 20-30%. Increases in the DV shunting rate are a general adaptational mechanism to fetal distress. Hypoxia results in a significant increase in the DV shunting rate, most probably in order to ensure an adequate supply of oxygen and glucose to vitally important organs such as the brain and heart. The mechanism of blood flow redistribution between the fetal liver and the DV is still a matter of debate. The isthmic portion of the DV contains less smooth muscle tissue than the intrahepatic branches of the portal vein, which in vitro react more forcefully in response to catecholamines than the DV. In growth-restricted human fetuses DV shunting is increased and the umbilical blood supply to the fetal liver is reduced. The long-term reduction of the hepatic blood supply may be involved in fetal growth restriction. The occlusion of the DV leads to a significant increase in cell proliferation in fetal skeletal muscle, heart, kidneys and liver, and possibly to an increase in insulin-like growth factor (IGF)-I and -II mRNA expression in the fetal liver. These findings hint at the possible role of the perfusion of the fetal liver in the control of the growth process. The quantification of DV shunting by Doppler velocimetry may improve the early recognition of fetal compromise in prenatal medicine. In this Review we summarize the published data on the anatomical structure and histology of the DV, the mechanisms of regulation of DV shunting, its role in fetal survival and growth and the possible use of the measurement of DV shunting in clinical practice.
AB - The fetal liver is located at the crossroads of the umbilical venous circulation. Anatomically, the ductus venosus (DV) and the intrahepatic branches of the portal vein are arranged in parallel. The actual DV shunting rate, i.e. the percentage of umbilical blood flow entering the DV measured by Doppler velocimetry, seems to be lower than that estimated using radioactively-labeled microspheres. In human fetuses the DV shunting rate is about 20-30%. Increases in the DV shunting rate are a general adaptational mechanism to fetal distress. Hypoxia results in a significant increase in the DV shunting rate, most probably in order to ensure an adequate supply of oxygen and glucose to vitally important organs such as the brain and heart. The mechanism of blood flow redistribution between the fetal liver and the DV is still a matter of debate. The isthmic portion of the DV contains less smooth muscle tissue than the intrahepatic branches of the portal vein, which in vitro react more forcefully in response to catecholamines than the DV. In growth-restricted human fetuses DV shunting is increased and the umbilical blood supply to the fetal liver is reduced. The long-term reduction of the hepatic blood supply may be involved in fetal growth restriction. The occlusion of the DV leads to a significant increase in cell proliferation in fetal skeletal muscle, heart, kidneys and liver, and possibly to an increase in insulin-like growth factor (IGF)-I and -II mRNA expression in the fetal liver. These findings hint at the possible role of the perfusion of the fetal liver in the control of the growth process. The quantification of DV shunting by Doppler velocimetry may improve the early recognition of fetal compromise in prenatal medicine. In this Review we summarize the published data on the anatomical structure and histology of the DV, the mechanisms of regulation of DV shunting, its role in fetal survival and growth and the possible use of the measurement of DV shunting in clinical practice.
M3 - SCORING: Zeitschriftenaufsatz
VL - 27
SP - 452
EP - 461
JO - ULTRASOUND OBST GYN
JF - ULTRASOUND OBST GYN
SN - 0960-7692
IS - 4
M1 - 4
ER -