Percutaneously adjustable portal vein banding device could prevent post-operative liver failure – Artificial control of portal venous flow is the key to a new therapeutic world

2009 ◽  
Vol 73 (5) ◽  
pp. 640-650 ◽  
Author(s):  
Julien Reyal ◽  
Shinji Uemoto
Keyword(s):  
Portal Vein ◽  
Liver Failure ◽  
Portal Venous Flow ◽  
Venous Flow ◽  
Artificial Control

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.

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.

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.

scholarly journals Multidisciplinary treatment of left hepatic artery pseudoaneurysm after hepatobiliary resection for gallbladder cancer: a case report

2019 ◽  
Vol 5 (1) ◽  
Author(s):  
Ryusei Yamamoto ◽  
Teiichi Sugiura ◽  
Yukiyasu Okamura ◽  
Takaaki Ito ◽  
Yusuke Yamamoto ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Portal Vein ◽  
Liver Failure ◽  
Hepatic Artery ◽  
Remnant Liver ◽  
Left Hepatic Artery ◽  
Artery Pseudoaneurysm ◽  
Hepatobiliary Resection ◽  
Portal Vein Arterialization ◽  
Arterial Inflow

Abstract Background When a postoperative hepatic artery pseudoaneurysm develops after massive hepatectomy, both an intervention for the pseudoaneurysm and patency of hepatic artery should be considered because occlusion of the residual hepatic artery results in critical liver failure. However, the treatment strategy for a pseudoaneurysm of the hepatic artery after hepatobiliary resection is not well established. Case presentation A 65-year-old woman underwent right hepatectomy, extrahepatic duct resection, and portal vein resection, for gallbladder cancer. Although the patient had an uneventful postoperative course, computed tomography on postoperative day 6 showed a 6-mm pseudoaneurysm of the hepatic artery. Angiography revealed the pseudoaneurysm located on the bifurcation of the left hepatic artery to the segment 2 artery plus the segment 3 artery and 4 artery. Stent placement in the left hepatic artery was not feasible because the artery was too narrow, and coiling of the pseudoaneurysm was associated with a risk of occluding the left hepatic artery and inducing critical liver failure. Therefore, portal vein arterialization constructed by anastomosing the ileocecal artery and vein was performed prior to embolization of the pseudoaneurysm to maintain the oxygen level of the remnant liver, even if the left hepatic artery was accidentally occluded. The pseudoaneurysm was selectively embolized without occlusion of the left hepatic artery, and the postoperative laboratory data were within normal limits. Although uncontrollable ascites due to portal hypertension occurred, embolization of the ileocolic shunt rapidly resolved it. The patient was discharged on postoperative day 45. Conclusion Portal vein arterialization prior to embolization of the aneurysm may be a feasible therapeutic strategy for a pseudoaneurysm that develops after hepatectomy for hepatobiliary malignancy to guarantee arterial inflow to the remnant liver. Early embolization of arterioportal shunting after confirmation of arterial inflow to the liver should be performed to prevent morbidity induced by portal hypertension.

scholarly journals Changes in Hepatic Hemodynamics due to Primary Liver Tumours

HPB Surgery ◽  
1996 ◽  
Vol 9 (4) ◽  
pp. 245-248 ◽  
Author(s):  
F. Jakab ◽  
Z. Ráth ◽  
F. Schmal ◽  
P. Nagy ◽  
J. Faller
Keyword(s):  
Hepatocellular Carcinoma ◽  
Blood Flow ◽  
Hepatic Artery ◽  
Hepatic Blood Flow ◽  
Primary Hepatocellular Carcinoma ◽  
Portal Venous Flow ◽  
Venous Flow ◽  
Control Value ◽  
Early Results ◽  
Total Hepatic Blood Flow

Data regarding the afferent circulation of the liver in patients with primary hepatocellular carcinoma are controversial, we have carried out measurement of hepatic arterial and portal venous flow intraoperatively by transit time ultrasonic volume flowmetry. In patients with primary hepatocellular carcinoma the hepatic artery flow increased to 0.55±0.211 compared with the control value of 0.37±0.102 1/min. (p<0.01). The portal venous flow decreased from 0.61±0.212 l/min, to 0.47±l/min. p<0.01). Due to the opposite changes in the afferent circulation the total hepatic blood flow did not change significantly, compared with controls.The ratio of hepatic arterial flow to portal vein flow increased to 1.239±0.246 in patients with hepatocellular carcinoma, which is double of the control value (0.66±0.259 l/min). After resection this ratio did not change.The resection did not alter hepatic artery or portal venous flow significantly, although the total hepatic blood flow decreased significantly (p<0.01).On the basis of our early results it is possible that the ratio of the two circulations may be to deel measured with doppler ultrasound and provide diagnostic information.

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