Cardiac anomalies associated with congenital absence of the portal vein

1999 ◽  
Vol 9 (5) ◽  
pp. 522-525 ◽  
Author(s):  
Martial Massin ◽  
Alain Verloes ◽  
Paul Jamblin
Keyword(s):  
Portal Vein ◽  
Right Atrium ◽  
Venous Return ◽  
Cardiac Development ◽  
Congenital Absence ◽  
Portal Venous Flow ◽  
Venous Flow ◽  
Cardiac Defects ◽  
Cardiac Anomalies ◽  
The Right

AbstractThe authors discovered congenital absence of the portal vein, with visceral venous return to the right atrium, in a 5-year-old girl with aortic valvar stenosis. Interestingly, of the 19 patients, it was discovered that 11 reported with portal venous agenesis also had cardiac defects. We have, therefore, investigated the hypothesis that the congenital absence of the portal vein and the associated cardiac malformations may result from a similar embryologic insult, and that cardiac development may be affected by the systemic diversion of portal venous flow.

Congenital Absence of the Right Pericardium Associated With Herniation of the Right Atrium

1970 ◽  
Vol 135 (7) ◽  
pp. 557-559 ◽  
Author(s):  
Nicolos T. Volenti ◽  
Melvin J. Spicer ◽  
David N. Bramwit ◽  
Ferdinand J. Montegut ◽  
William P. Nelson
Keyword(s):  
Right Atrium ◽  
Congenital Absence ◽  
The Right

scholarly journals Hepatocellular Carcinoma With Tumor Thrombus Occupying the Right Atrium and Portal Vein

Medicine ◽  
2015 ◽  
Vol 94 (34) ◽  
pp. e1049 ◽  
Author(s):  
Xin Luo ◽  
Binhao Zhang ◽  
Shuilin Dong ◽  
Bixiang Zhang ◽  
Xiaoping Chen
Keyword(s):  
Hepatocellular Carcinoma ◽  
Portal Vein ◽  
Right Atrium ◽  
Tumor Thrombus ◽  
The Right

Systemic and splanchnic haemodynamic effects of pentifylline in rats with portal hypertension

1992 ◽  
Vol 83 (1) ◽  
pp. 41-45 ◽  
Author(s):  
M. Dagenais ◽  
G. Pomier-Layrargues ◽  
B. Rocheleau ◽  
L. Giroux ◽  
P.-M. Huet
Keyword(s):  
Cardiac Output ◽  
Portal Hypertension ◽  
Portal Vein ◽  
Portal Pressure ◽  
Reference Sample ◽  
Peripheral Resistance ◽  
Haemodynamic Effects ◽  
Portal Vein Ligation ◽  
Portal Venous Flow ◽  
Venous Flow

1. The systemic and splanchnic haemodynamic effects of pentifylline (40 mg/kg body weight intravenously) were assessed in rats with portal hypertension associated either with CCl4-induced cirrhosis (n= 13) or portal vein ligation (n=13). 2. Heparinized catheters were placed into the portal vein, inferior vena cava, aorta and left ventricle with exits from the neck. Haemodynamic studies were performed 4 h after consciousness was regained. Cardiac output and regional blood flows were measured using radiolabelled microspheres and the reference sample method in seven rats in each group; portal-systemic shunting was measured using microsphere injection in the ileo-colic vein in six rats in each group. 3. Forty-five minutes after injection, pentifylline had no effect on mean arterial pressure, cardiac output, peripheral resistance, portal venous flow, hepatic artery flow or portal-systemic shunting in either group of rats with portal hypertension. The drug lowered portal pressure (−18%) in cirrhotic rats, but not in portal-vein-ligated rats. 4. These data demonstrate that pentifylline lowers portal pressure in cirrhotic rats without affecting portal venous flow and portal-systemic shunting; this effect is possibly mediated by changes in intrahepatic resistance related to the effects of pentifylline on blood viscosity and/or on intrahepatic vasomotor tone.

scholarly journals Magnetic Resonance Elastography and Portal Hypertension: Influence of the Portal Venous Flow on the Liver Stiffness

2021 ◽  
Author(s):  
Simon Chatelin ◽  
Raoul Pop ◽  
Céline Giraudeau ◽  
Khalid Ambarki ◽  
Ning Jin ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Magnetic Resonance ◽  
Portal Vein ◽  
Peak Flow ◽  
Peak Velocity ◽  
Liver Stiffness ◽  
Portal Venous Flow ◽  
Venous Flow ◽  
Velocity Magnitude ◽  
Magnetic Resonance Imaging Mri

The invasive measurement of the hepatic venous pressure gradient is still considered as the reference method to assess the severity of portal hypertension. Even though previous studies have shown that the liver stiffness measured by elastography could predict portal hypertension in patients with chronic liver disease, the mechanisms behind remain today poorly understood. The main reason is that the liver stiffness is not specific to portal hypertension and is also influenced by concomitant pathologies, such as cirrhosis. Portal hypertension is also source of a vascular incidence, with a substantial diversion of portal venous blood to the systemic circulation, bypassing the liver. This study focuses on this vascular effect of portal hypertension. We propose to generate and control the portal venous flow (to isolate the modifications in the portal venous flow as single effect of portal hypertension) in an anesthetized pig and then to quantify its implications on liver stiffness by an original combination of MRE and 4D-Flow Magnetic Resonance Imaging (MRI). A catheter balloon is progressively inflated in the portal vein and the peak flow, peak velocity magnitude and liver stiffness are quantified in a 1.5T MRI scanner (AREA, Siemens Healthcare, Erlangen, Germany). A strong correlation is observed between the portal peak velocity magnitude, the portal peak flow or the liver stiffness and the portal vein intraluminal obstruction. Moreover, the comparison of mechanical and flow parameters highlights a correlation with the possibility of identifying linear relationships. These results give preliminary indications about how liver stiffness can be affected by portal venous flow and, by extension, by hypertension.

scholarly journals Hepatocellular carcinoma with tumor thrombus extends to the right atrium and portal vein: A case report

2020 ◽  
Vol 12 (11) ◽  
pp. 1128-1135
Author(s):  
Diego Gomez-Puerto ◽  
Oriol Mirallas ◽  
Judit Vidal-González ◽  
Victor Vargas
Keyword(s):  
Hepatocellular Carcinoma ◽  
Case Report ◽  
Portal Vein ◽  
Right Atrium ◽  
Tumor Thrombus ◽  
The Right

Hepatic venular pressures of rats, dogs, and rabbits

1991 ◽  
Vol 261 (3) ◽  
pp. G539-G547 ◽  
Author(s):  
H. G. Bohlen ◽  
R. Maass-Moreno ◽  
C. F. Rothe
Keyword(s):  
Inferior Vena Cava ◽  
Portal Vein ◽  
Inferior Vena ◽  
Venous Pressure ◽  
Vena Cava ◽  
Portal Venous Flow ◽  
Venous Flow ◽  
Norepinephrine Infusion ◽  
Venous Resistance ◽  
Venous Vasculature

We tested the hypotheses that the hepatic venule pressures (Phv), just downstream from the hepatic sinusoids, are closely similar (less than 2 mmHg) either to the portal venous pressure (Ppv), indicating a high hepatic venous resistance, or to the inferior vena cava (Pivc) pressure, indicating a high portal-sinusoidal venous resistance, as reported by previous investigators. A micropipette servo-null pressure measurement technique was used with rats, dogs, and rabbits. Phv, referred to the anatomic level of the vena cava, averaged 5.1 +/- 1.0, 6.4 +/- 1.1, and 5.4 +/- 1.0 (SD) mmHg in the rats, puppies, and rabbits, respectively. Ppv averaged 8.0 +/- 1.4, 10.8 +/- 2.2, and 7.4 +/- 1.5 mmHg, respectively. Norepinephrine infusion into the portal vein (1-5 micrograms.min-1.kg-1) caused Ppv to increase and the portal venous flow to decrease but did not significantly affect Phv. The hepatic venous circuit contributed 44 +/- 17% (rats) and 31 +/- 26% (dogs) of the total liver venous vascular resistance under control conditions. We conclude that the portal and sinusoidal vasculatures are the dominant, but not exclusive, resistance sites of the liver venous vasculature both at rest and during norepinephrine-induced vasoconstriction.

Atrial Septal Displacement for Repair of Anomalous Pulmonary Venous Return Into the Right Atrium

1998 ◽  
Vol 65 (4) ◽  
pp. 1110-1114 ◽  
Author(s):  
Takeshi Hiramatsu ◽  
Yoshinori Takanashi ◽  
Yasuharu Imai ◽  
Shuichi Hoshino ◽  
Kazuhiro Seo ◽  
...  
Keyword(s):  
Right Atrium ◽  
Venous Return ◽  
Anomalous Pulmonary Venous Return ◽  
The Right

scholarly journals Effect of breathing on venous return during delayed cord clamping: an observational study

2021 ◽  
pp. fetalneonatal-2020-321431
Author(s):  
Emma Brouwer ◽  
Ronny Knol ◽  
Annie Kroushev ◽  
Thomas Van Den Akker ◽  
Stuart B Hooper ◽  
...  
Keyword(s):  
Flow Velocity ◽  
Right Atrium ◽  
Spontaneous Breathing ◽  
Venous Return ◽  
Vena Cava ◽  
Ductus Venosus ◽  
Delayed Cord Clamping ◽  
Cord Clamping ◽  
Digital Format ◽  
The Right

ObjectiveTo investigate the effect of spontaneous breathing on venous return in term infants during delayed cord clamping at birth.MethodsEchocardiographic ultrasound recordings were obtained directly after birth in healthy term-born infants. A subcostal view was used to obtain an optimal view of the inferior vena cava (IVC) entering the right atrium, including both the ductus venosus (DV) and the hepatic vein (HV). Colour Doppler was used to assess flow direction and flow velocity. Recordings continued until the umbilical cord was clamped and were stored in digital format for offline analyses.ResultsUltrasound recordings were obtained in 15 infants, with a median (IQR) gestational age of 39.6 (39.0–40.9) weeks and a birth weight of 3560 (3195–4205) g. Flow was observed to be antegrade in the DV and HV in 98% and 82% of inspirations, respectively, with flow velocity increasing in 74% of inspirations. Retrograde flow in the DV was observed sporadically and only occurred during expiration. Collapse of the IVC occurred during 58% of inspirations and all occurred caudal to the DV inlet (100%).ConclusionSpontaneous breathing was associated with collapse of the IVC and increased antegrade DV and HV flow velocity during inspiration. Therefore, inspiration appears to preferentially direct blood flow from the DV into the right atrium. This indicates that inspiration could be a factor driving placental transfusion in infants.

Mechanism of the Increased Venous Return and Cardiac Output Caused by Epinephrine

1957 ◽  
Vol 192 (1) ◽  
pp. 126-130 ◽  
Author(s):  
Arthur C. Guyton ◽  
Arthur W. Lindsey ◽  
Berry Abernathy ◽  
Jimmy B. Langston
Keyword(s):  
Cardiac Output ◽  
Pressure Gradient ◽  
Spinal Anesthesia ◽  
Right Atrium ◽  
Venous Return ◽  
Operating Conditions ◽  
Total Spinal Anesthesia ◽  
Vascular Walls ◽  
The Mean ◽  
The Right

The effect of epinephrine on venous return has been measured in 11 dogs under total spinal anesthesia. The mechanism by which epinephrine increases venous return seems to be to increase the tone of the vascular walls thereby increasing the mean circulatory pressure. This in turn increases the pressure gradient forcing blood from the systemic vessels toward the right atrium. By equating the recorded venous return curves with curves that depict the effect of epinephrine on the heart's ability to pump blood, it is shown that under normal operating conditions cardiac output is determined far more by the tendency for blood to return to the heart than by the heart's ability to pump blood.

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