scholarly journals The Relationship between Portal Venous and Hepatic Arterial Blood Flow. I. Experimental Liver Transplantation

HPB Surgery ◽  
1996 ◽  
Vol 10 (1) ◽  
pp. 21-26 ◽  
Author(s):  
F. Jakab ◽  
I. Sugár ◽  
Z. Ráth ◽  
P. Nágy ◽  
J. Faller
Keyword(s):  
Liver Transplantation ◽  
Portal Vein ◽  
Hepatic Artery ◽  
Portal Pressure ◽  
Arterial Blood Flow ◽  
Portal Flow ◽  
Continuous Increase ◽  
Arterial Blood ◽  
Artery Flow ◽  
The Relationship

The relationship between the changes in portal venous and hepatic arterial blood flows, in the liver is a much disputed question, it has tremendous significance in the practice of transplantation, and an explanation has been available since 1981, when Lautt published the so-caled “adenosine washout theory”. According to our earlier observations the decrease of portal pressure or flow consistently led to an increase in hepatic artery flow. At the same time changes in hepatic artery flow or pressure seemed to produce only inconsistent effects on the portal circulation. In the present experiments liver transplantation (OLTX) was carried out on mongrel dogs by Starzl's method. Electromagnetic flow probes were placed on the hepatic artery and the portal vein before removal of recipient’s liver, and after completion of all vascular anastomoses to the newly inserted liver, during the recirculatory phase of OLTX. The flow probes were connected to a Hellige electromagnetic flowmeter, portal venous and systemic arterial pressures were also recorded.The control HAF was 241±23 ml/min, the average PVF was 517±47 ml/min before removal of the recipients's liver. In the recirculatory phase the HAF increased, by 71±12% (p < 0.001). The PVF decreased in most animals after OLTX. The decrease was in average –40.2±3.5% (p < 0.001). The THBF calculated by adding the HAF and PVF showed a small, but not significant decrease during recirculation.The systemic arterial pressure decreased slightly and portal vein pressure rose in most animals after OLTX. There was a substantial increase in portal inflow resistance and prehepatic arteriolar resistance and a decrease in hepatic artery resistance. The decrease of PVF after OLTX can be explained by progressive fluid accumulation in the liver parenchyma and increased sinusoidal and portal inflow resistance. The prolonged and continuous increase in hepatic artery flow during the recirculatory phase of OLTX may be due to the decrease of portal flow. The exact mechanism, by which a change in portal flow leads to arteriolar dilatation, can be most probably explained by the “adenosine washout theory” of Lautt.

scholarly journals Hepatic Artery Pseudoaneurysm Rupture with Acute Portal Vein Occlusion Treated with Coronary Stent Graft and Trans-splenic Portal Vein Stenting

2019 ◽  
Vol 03 (01) ◽  
pp. 062-064
Author(s):  
Stephen Allison ◽  
Arthie Jeyakumar ◽  
Guy Johnson ◽  
Matthew Kogut
Keyword(s):  
Portal Vein ◽  
Hepatic Artery ◽  
Stent Graft ◽  
Coronary Stent ◽  
Arterial Blood Flow ◽  
Artery Pseudoaneurysm ◽  
Portal Vein Occlusion ◽  
Bleeding Vessel ◽  
Vein Occlusion ◽  
Arterial Blood

AbstractDelayed massive hemorrhage following pancreaticoduodenectomy is a potentially fatal condition. These patients are often not surgical candidates, and endovascular therapy is the primary option of treatment, usually trans-arterial embolization. However, the bleeding vessel can occasionally be treated with a stent graft rather than embolization. This decreases the risk of hepatic necrosis by preserving hepatic arterial blood flow, particularly in patients with compromised portal veins. The authors present a brief case report of delayed pseudoaneurysm rupture from a replaced proper hepatic artery after pancreaticoduodenectomy with resultant portal vein occlusion, caused by hematoma mass effect. The hepatic artery was treated with a coronary stent. During the same session, trans-splenic portal vein stenting was done.

Hepatic artery buffer response following left portal vein ligation: its role in liver tissue homeostasis

1999 ◽  
Vol 277 (5) ◽  
pp. G1000-G1007 ◽  
Author(s):  
B. Rocheleau ◽  
C. Éthier ◽  
R. Houle ◽  
P. M. Huet ◽  
M. Bilodeau
Keyword(s):  
Portal Vein ◽  
Hepatic Artery ◽  
Liver Tissue ◽  
Arterial Flow ◽  
Portal Vein Ligation ◽  
Portal Flow ◽  
Left Liver ◽  
Compensatory Increase ◽  
Left Portal Vein ◽  
Artery Flow

Occlusion of a lobar portal vein is known to induce atrophy of downstream liver lobes and hypertrophy of contralateral lobes. Changes in portal flow are known to be compensated by changes in hepatic arterial flow, thus defining the hepatic artery buffer response (HABR). To understand the role of liver flow in liver atrophy, we measured portal flow and hepatic artery flow after different degrees of left portal vein stenosis (LPVS). Surgery was performed to obtain 0, 43, 48, 59, 68, 72, 78, and 100% LPVS. Systemic and splanchnic blood flows were measured at 4 h or 7 days after surgery using radiolabeled microspheres. At 4 h, LPVS produced no changes in systemic hemodynamics. Increasing degrees of LPVS produced a significant decrease in left portal flow ( P < 0.0001) and a fully compensatory increase in right portal flow ( P < 0.0001) without significantly affecting total portal flow. Left hepatic artery flow increased by 210% ( P = 0.002), and right hepatic artery flow decreased by 67% ( P = 0.05) after full LPVS. There was a significant inverse correlation between portal and arterial flow changes induced by different degrees of LPVS in the left ( r 2 = 0.61) and right ( r 2 = 0.41) lobes. Despite this HABR, we observed a reduction in left liver flow (−45%; P = 0.01) and an increase in right liver flow (+230%; P = 0.01) with 100% LPVS. At 7 days, a significant decrease in the weight of left liver lobes (−75%; P < 0.0001) and a compensatory increase in the weight of the right lobes (+210%; P < 0.0001) were observed with 100% LPVS. Left and right liver flows were similar to results measured at 4 h, and HABR was still present. However, when expressed per gram of liver, liver flows were identical to results obtained with sham animals. Reduction in lobar portal flow is accompanied by an increase in ipsilateral hepatic artery flow and a compensatory increase in portal flow to the rest of the liver. In a given lobe, when compensatory HABR is overcome, liver weight changes occur so that at the end total liver flow per gram of liver tissue is restored. This suggests that in normal conditions liver flow is a major regulator of liver volume.

Participation of adrenoceptors in liver blood flow regulation in anesthetized dogs

1987 ◽  
Vol 253 (5) ◽  
pp. H1053-H1058
Author(s):  
N. Terada ◽  
S. Koyama ◽  
J. Horiuchi ◽  
T. Takeuchi
Keyword(s):  
Blood Flow ◽  
Portal Vein ◽  
Hepatic Artery ◽  
Vascular Resistance ◽  
Adrenergic Receptors ◽  
Liver Blood Flow ◽  
Arterial Blood Flow ◽  
Tissue Blood Flow ◽  
Intact Group ◽  
Arterial Blood

We evaluated involvement of adrenergic receptors in the responses of the hepatic vasculature to reduction either of portal venous flow or hepatic arterial inflow. Portal vein occlusion caused an increase in hepatic arterial blood flow (HAF) and decreases in hepatic arterial pressure (HAP) and hepatic arterial vascular resistance (HAR) in the intact group. After pretreatment with either yohimbine or prazosin, but not propranolol, occlusion of the portal vein produced a greater decrease in HAP as compared with that in the intact group. No significant changes in HAF, HAR, or hepatic tissue blood flow (HTF) occurred after the treatment. These results indicate that the compensatory response of the hepatic arterial vasculature to altered portal blood flow (PVF) is regulated independently of the intrahepatic adrenergic receptors. Hepatic arterial occlusion caused a significant decrease in portal venous pressure, PVF, and HTF. Portal venous vascular resistance (PVR) was reduced slightly, but not significantly. After pretreatment with either yohimbine or prazosin, but not propranolol, occlusion of the hepatic artery produced an opposite effect: to increase PVF and significantly decrease PVR. These results indicate that intrahepatic alpha-adrenoceptors participate in the regulation of portal vascular tone to maintain portal vein pressure at a steady level, when inflow from the hepatic artery is reduced.

scholarly journals Providing Arterial Supply to the Liver Graft with Recipient Splenic Artery in Living Donor Liver Transplantation: Case Report

2020 ◽  
pp. 1-3
Author(s):  
Kaleem Ullah ◽  
Shams Uddin ◽  
Hala Izzu ◽  
Kaleem Ullah ◽  
Abdul Wahab Dogar ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Case Report ◽  
Hepatic Artery ◽  
Splenic Artery ◽  
Surgical Techniques ◽  
Arterial Blood Flow ◽  
Liver Graft ◽  
Artery Dissection ◽  
Arterial Blood ◽  
Operative Recovery

Hepatic arterial reconstruction is an important step in graft implantation in liver transplant procedure. Hepatic arterial anastomosis always demands meticulous and highly skilled surgical techniques to provide adequate blood supply to the graft. Hepatic arterial intimal dissection in liver transplantation is although a rare but documented complication, with incidence of less than 5%, but having dreadful complications. To overcome this complication of Recipient hepatic artery dissection, various techniques have been described by different authors. Here, in this case report we are describing technique of utilization of transposed recipient splenic artery for graft arterial inflow where native hepatic artery was dissected up to common hepatic artery. Post-operative recovery was uneventful and on follow up, patient was absolutely fine. So, recipient splenic artery is a safe alternative option in such complex situations for providing arterial blood flow to the graft and moreover it avoids the burden of extra anastomosis which is required in conduit technique.

H2S contributes to the hepatic arterial buffer response and mediates vasorelaxation of the hepatic artery via activation of KATP channels

2008 ◽  
Vol 295 (6) ◽  
pp. G1266-G1273 ◽  
Author(s):  
Nikolai Siebert ◽  
Daniel Cantré ◽  
Christian Eipel ◽  
Brigitte Vollmar
Keyword(s):  
Blood Flow ◽  
Portal Vein ◽  
Hepatic Artery ◽  
Buffer Capacity ◽  
Venous Blood ◽  
Control Level ◽  
Vena Cava ◽  
Arterial Blood Flow ◽  
Venous Blood Flow ◽  
Arterial Blood

Hepatic blood supply is uniquely regulated by the hepatic arterial buffer response (HABR), counteracting alterations of portal venous blood flow by flow changes of the hepatic artery. Hydrogen sulfide (H2S) has been recognized as a novel signaling molecule with vasoactive properties. However, the contribution of H2S in mediating the HABR is not yet studied. In pentobarbital-anesthetized and laparotomized rats, flow probes around the portal vein and hepatic artery allowed for assessment of the portal venous (PVBF) and hepatic arterial blood flow (HABF) under baseline conditions and stepwise reduction of PVBF for induction of HABR. Animals received either the H2S donor Na2S, DL-propargylglycine as inhibitor of the H2S synthesizing enzyme cystathionine-γ-lyase (CSE), or saline alone. Additionally, animals were treated with Na2S and the ATP-sensitive potassium channel (KATP) inhibitor glibenclamide or with glibenclamide alone. Na2S markedly increased the buffer capacity to 27.4 ± 3.0% ( P < 0.05 vs. controls: 15.5 ± 1.7%), whereas blockade of H2S formation by DL-propargylglycine significantly reduced the buffer capacity (8.5 ± 1.4%). Glibenclamide completely reversed the H2S-induced increase of buffer capacity to the control level. By means of RT-PCR, Western blot analysis, and immunohistochemistry, we observed the expression of both H2S synthesizing enzymes (CSE and cystathionine-β-synthase) in aorta, vena cava, hepatic artery, and portal vein, as well as in hepatic parenchymal tissue. Terminal branches of the hepatic afferent vessels expressed only CSE. We show for the first time that CSE-derived H2S contributes to HABR and partly mediates vasorelaxation of the hepatic artery via activation of KATP channels.

scholarly journals A New Method to Measure Portal Venous and Hepatic Arterial Blood Flow Patients Intraoperatively

HPB Surgery ◽  
1996 ◽  
Vol 9 (4) ◽  
pp. 239-243 ◽  
Author(s):  
F. Jakab ◽  
Z. Ráth ◽  
F. Schmal ◽  
P. Nagy ◽  
J. Faller
Keyword(s):  
Hepatic Artery ◽  
Arterial Flow ◽  
Arterial Blood Flow ◽  
Portal Venous Flow ◽  
Hepatic Arterial Flow ◽  
Venous Flow ◽  
Venous Circulation ◽  
Arterial Blood ◽  
Temporary Occlusion ◽  
Artery Flow

The intraoperative measurement of the afferent circulation of the liver, namely the hepatic artery flow and portal venous flow was carried out upon 14 anesthetized patients having carcinoma in the splanchnic area, mainly in the head of the pancreas by means of transit time ultrasonic volume flowmeter. The hepatic artery flow, portal venous flow and total hepatic flow were 0.377±0.10; 0.614±0.21; 0.992±0.276 l/min respectively.The ratio of hepatic arterical flow to portal venous flow was 0.66±0.259 There was a sharp, significant increase in hepatic arterial flow (29.8±6.1%, p<0,01) after the temporary occlusion of the portal vein, while the temporary occlusion of hepatic artery did not have any significant effect on portal venous circulation. The interaction between hepatic arterial flow and portal venous flow is a much disputed question, but according to the presented data here, it is unquestionable, that the decrease of portal venous flow immediately results a significant increase in hepatic artery circulation.

Sufficient hepatic artery flow compensates for poor portal vein flow after liver transplantation in patients with portal vein thrombosis

2019 ◽  
Vol 33 (11) ◽  
Author(s):  
Kazunari Sasaki ◽  
John C. McVey ◽  
Daniel J. Firl ◽  
Nikolaos Andreatos ◽  
Amika Moro ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Portal Vein ◽  
Hepatic Artery ◽  
Portal Vein Thrombosis ◽  
Portal Vein Flow ◽  
Vein Thrombosis ◽  
Artery Flow

scholarly journals Hemodynamic profile and tissular oxygenation in orthotopic liver transplantation: Influence of hepatic artery or portal vein revascularization of the graft

2006 ◽  
Vol 12 (11) ◽  
pp. 1607-1614 ◽  
Author(s):  
Carlos Moreno ◽  
Antoni Sabaté ◽  
Joan Figueras ◽  
Imma Camprubí ◽  
Antonia Dalmau ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Portal Vein ◽  
Hepatic Artery ◽  
Orthotopic Liver Transplantation ◽  
Hemodynamic Profile
Sign in / Sign up

Export Citation Format

Share Document