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

Author(s):  
Simon Chatelin ◽  
Raoul Pop ◽  
Céline Giraudeau ◽  
Khalid Ambarki ◽  
Ning Jin ◽  
...  

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.

1992 ◽  
Vol 83 (1) ◽  
pp. 41-45 ◽  
Author(s):  
M. Dagenais ◽  
G. Pomier-Layrargues ◽  
B. Rocheleau ◽  
L. Giroux ◽  
P.-M. Huet

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.


2019 ◽  
Vol 9 ◽  
pp. 20 ◽  
Author(s):  
Daniel C. Oppenheimer ◽  
Luann Jones ◽  
Ashwani Sharma

Transjugular intrahepatic portosystemic shunt (TIPS) is a widely accepted option for treating the complications of portal hypertension. The procedure involves creating a communication between the portal and hepatic venous systems using imaging guidance, thereby diverting the portal venous flow and reducing the portosystemic gradient. However, as with any procedure, TIPS insertion is not without potential complications. We present a case of a 37-year-old female who developed a hepatic artery pseudoaneurysm following the placement of a TIPS which was successfully treated with percutaneous thrombin injection.


1998 ◽  
Vol 31 (9) ◽  
pp. 1991-1995
Author(s):  
Hidefumi Baba ◽  
Katsunori Tanaka ◽  
Shigenao Kan ◽  
Fumio Suzuki ◽  
Hitoshi Otaka ◽  
...  

2020 ◽  
Vol 36 (6) ◽  
pp. 567-571
Author(s):  
Danielle E. Cain ◽  
Sharlette Anderson

Portal hypertension is a result of an increase in intrahepatic resistance in the main portal vein. The Meso-Rex shunt is used to bypass the obstructed portal vein and restore the venous flow into the liver. This procedure alleviates the need for a hepatic transplant. The Meso-Rex shunt has proven to be an effective treatment for extrahepatic portal vein obstruction, thus saving children from a complete transplant. There are variants to this bypass surgery, and sonography is commonly used to assess the condition pre- and postoperatively. In this case, the shunt was uniquely different from the typical Meso-Rex bypass surgery. Particular vasculature made it imperative for the sonographer to review the prior sonograms and review the chart information before preforming the examination. It should also be noted that sonographers must adapt the protocols to give the utmost treatment.


1991 ◽  
Vol 261 (3) ◽  
pp. G539-G547 ◽  
Author(s):  
H. G. Bohlen ◽  
R. Maass-Moreno ◽  
C. F. Rothe

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.


2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Federica Pulvirenti ◽  
Ilaria Pentassuglio ◽  
Cinzia Milito ◽  
Michele Valente ◽  
Adriano De Santis ◽  
...  

Background and Aim. Portal hypertension has been reported in association with acquired and primary immune deficiencies without a comprehensive description of associated spleno-portal axis abnormalities. Pathological mechanisms are poorly defined.Methods. Observational, single centre study with the aim of assessing the prevalence of spleno-portal axis abnormalities in an unselected cohort of 123 patients with primary antibody deficiencies and without known causes of liver diseases regularly followed up for a mean time of 18 ± 14 years. A cumulative period of 1867 patients-year was analysed. Clinical and immunological data, abdominal ultrasounds, CT scans, and endoscopy features were included in the analysis.Results. Twenty-five percent of patients with primary antibody deficiencies had signs of portal vein enlargement but only 4% of them had portal hypertension, with portal systemic collaterals. Liver biopsies showed liver sinusoids congestive dilatation, endothelization, and micronodularity fulfilling the criteria for noncirrhotic portal hypertension. Patients with portal vein enlargement had severe clinical and immunological phenotypes.Conclusions. In primary antibody deficient patients, infections, inflammations, splenomegaly, increased blood venous flow, and lymphocyte abnormalities contribute to establishment of liver damage possibly leading to noncirrhotic portal hypertension. Patients with primary antibody deficiency should be considered a good model to give insight into the pathological mechanisms underlying noncirrhotic portal hypertension.


1999 ◽  
Vol 9 (5) ◽  
pp. 522-525 ◽  
Author(s):  
Martial Massin ◽  
Alain Verloes ◽  
Paul Jamblin

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.


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