Portal branch ligation induces a hepatic arterial buffer response, microvascular remodeling, normoxygenation, and cell proliferation in portal blood-deprived liver tissue

Kollmar, Otto; Corsten, Marcus; Scheuer, Cláudia; Vollmar, Brigitte; Schilling, Martin K.; Menger, Michael D.

doi:10.1152/ajpgi.00503.2006

Cited by 52 publications

(44 citation statements)

References 33 publications

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“…37,38 Subsequently, rapid development of venous collaterals and formation of varices as well as cavernoma occur. These dilated venous collaterals exert external pressure and protrude into the thin and pliable CBD and the hepatic ducts ( Figure 1).…”

Section: Pathogenesismentioning

confidence: 99%

Portal Cavernoma Cholangiopathy: Consensus Statement of a Working Party of the Indian National Association for Study of the Liver

Dhiman

Saraswat

Valla

et al. 2014

Journal of Clinical and Experimental Hepatology

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Portal cavernoma cholangiopathy (PCC) is defined as abnormalities in the extrahepatic biliary system including the cystic duct and gallbladder with or without abnormalities in the 1st and 2nd generation biliary ducts in a patient with portal cavernoma. Presence of a portal cavernoma, typical cholangiographic changes on endoscopic or magnetic resonance cholangiography and the absence of other causes of these biliary changes like bile duct injury, primary sclerosing cholangitis, cholangiocarcinoma etc are mandatory to arrive a diagnosis. Compression by porto-portal collateral veins involving the paracholedochal and epicholedochal venous plexuses and cholecystic veins and ischemic insult due to deficient portal blood supply or prolonged compression by collaterals bring about biliary changes. While the former are reversible after porto-systemic shunt surgery, the latter are not. Majority of the patients with PCC are asymptomatic and approximately 21% are symptomatic. Symptoms in PCC could be in the form of long standing jaundice due to chronic cholestasis, or biliary pain with or without cholangitis due to biliary stones. Endoscopic retrograde cholangiography has no diagnostic role because it is invasive and is associated with risk of complications, hence it is reserved for therapeutic procedures. Magnetic resonance cholangiography and portovenography is a noninvasive and comprehensive imaging technique, and is the modality of choice for mapping of the biliary and vascular abnormalities in these patients. PCC is a progressive condition and symptoms develop late in the course of portal hypertension only in patients with severe or advanced changes of cholangiopathy. Asymptomatic patients with PCC do not require any treatment. Treatment of symptomatic PCC can be approached in a phased manner, coping first with biliary clearance by nasobiliary or biliary stent placement for acute cholangitis and endoscopic biliary sphincterotomy for biliary stone removal; second, with portal decompression by creating portosystemic shunt; and third, with persistent biliary obstruction by performing second-stage biliary drainage surgery such as hepaticojejunostomy or choledochoduodenostomy. Patients with symptomatic PCC have good prognosis after successful endoscopic biliary drainage and after successful shunt surgery. ( J CLIN EXP HEPATOL 2014;4:S2-S14)

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Section: Pathogenesismentioning

confidence: 99%

Portal Cavernoma Cholangiopathy: Consensus Statement of a Working Party of the Indian National Association for Study of the Liver

Dhiman

Saraswat

Valla

et al. 2014

Journal of Clinical and Experimental Hepatology

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“…37 However, most malignant tumors tolerate hypoxia quite well. 38 In addition, hypoxia may induce cellular changes that can result in more aggressive phenotypes with increased potential for local invasive growth, distant tumor spreading, and resistance to therapy.…”

Section: Cytokines and Growth Factorsmentioning

confidence: 99%

“…40 In the late phase after ligation, tissue remodeling takes place which is dominated by cell proliferation. 37 Hence, tumor proliferation may be promoted in this late phase after PVE.…”

Section: Cytokines and Growth Factorsmentioning

confidence: 99%

“…42 Clinical and experimental studies demonstrate a significant increase in hepatic arterial blood flow in the occluded liver lobes resulting from an increase in common hepatic arterial flow. 37,43 After portal vein occlusion, sinusoidal perfusion is derived almost totally from arterial blood supply. 44 Because liver tumors are mainly fed by the hepatic artery, the hepatic arterial buffer response potentially stimulates tumor growth in the embolized liver lobes.…”

Section: Alteration In Hepatic Blood Supplymentioning

confidence: 99%

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Induction of Tumor Growth After Preoperative Portal Vein Embolization: Is It a Real Problem?

et al. 2008

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Although preoperative portal vein embolization (PVE) is an effective means to increase future remnant liver (FRL) volume, little has been published on possible adverse effects. This review discusses the clinical and experimental evidence regarding the effect of PVE on tumor growth in both embolized and nonembolized liver lobes, as well as potential strategies to control tumor progression after PVE. A literature review was performed using MEDLINE with keywords related to experimental and clinical studies concerning PVE, portal vein ligation (PVL), and tumor growth. Cross-references and references from reviews were also checked. Clinical and experimental data suggest that tumor progression can occur after preoperative PVE in embolized and nonembolized liver segments. Clinical evidence indicating possible tumor progression in patients with colorectal metastases or with primary liver tumors is based on studies with small sample size. Although multiple studies demonstrated tumor progression, evidence concerning a direct increase in tumor growth rate as a result of PVE is circumstantial. Three possible mechanisms influencing tumor growth after PVE can be recognized, namely changes in cytokines or growth factors, alteration in hepatic blood supply and an enhanced cellular host response promoting local tumor growth after PVE. Post-PVE chemotherapy and sequential transcatheter arterial chemoembolization (TACE) before PVE have been proposed to reduce tumor mass after PVE. We conclude that tumor progression can occur after PVE in patients with colorectal metastases as well as in patients with primary liver tumors. However, further research is needed in order to rate this risk of tumor progression after PVE.Preoperative portal vein embolization (PVE) is an accepted intervention in patients requiring major liver resection in whom the estimated future remnant liver (FRL) is too small to allow safe resection.1,2 PVE induces atrophy of the embolized, tumor-bearing liver lobe while compensatory hypertrophy of the nonembolized lobe occurs, thereby increasing FRL volume and function.

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“…For monitoring of hepatic microvascular blood flow, laser Doppler fluxmetry (LDF; PeriFlux System 5000, Perimed, Stockholm, Sweden) was used [30,31]. Blood flow was measured by placing the laser Doppler probe on three different areas of the liver surface in the center of the right and the left lobe.…”

Section: Methodsmentioning

confidence: 99%

Hepatic Arterial Infusion with Tumor Necrosis Factor-α Induces Early Hepatic Hyperperfusion

Schäfer¹,

Sperling²,

Slotta³

et al. 2012

Eur Surg Res

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Background: Hepatic arterial infusion (HAI) has been developed for high-dose regional chemotherapy of unresectable liver metastases or primary liver malignancies. While it is well known that high concentrations of tumor necrosis factor (TNF)-α damage tumor blood perfusion, there is no information on whether autochthonous liver perfusion is affected by HAI with TNF-α. Therefore, we investigated the effects of HAI with TNF-α on hepatic macro- and microvascular perfusion. Methods: Swabian Hall pigs were randomized into three groups. HAI was performed with either 20 or 40 µg/kg body weight TNF-α (n = 6 each group). Saline-treated animals served as controls (n = 6). Analyses during a 2-hour post-HAI observation period included systemic hemodynamics, portal venous and hepatic arterial blood flow, portal venous pressure, and the blood flow in the hepatic microcirculation. Results: HAI with TNF-α caused a slight decrease of mean arterial blood pressure (p < 0.001), which was compensated by a moderate increase of heart rate (p < 0.001). No further systemic side effects of TNF-α were observed. HAI with TNF-α further caused a slight but not significant decrease of portal venous blood flow (p = 0.737) in both experimental groups, paralleled by an increase of hepatic arterial blood flow (p = 0.023, 20 µg/kg; p = 0.034, 40 µg/kg) resulting in an overall hepatic hyperperfusion. The hepatic hyperperfusion after HAI with 20 µg/kg TNF-α was more pronounced and associated with a 40% decrease of the blood flow in the hepatic microcirculation (p = 0.009). HAI with 40 µg/kg TNF-α was only associated with a temporary and moderate total hepatic hyperperfusion and did not affect the blood flow in the hepatic microcirculation. Conclusion: HAI with TNF-α causes a decrease of portal venous flow; however, this is overcompensated by an increased hepatic arterial blood flow, resulting in a total hepatic hyperperfusion. Moderate total hepatic hyperperfusion does not affect the blood flow in the hepatic microcirculation, while a persistent and more pronounced hyperperfusion may cause hepatic microcirculatory disturbances.

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Portal branch ligation induces a hepatic arterial buffer response, microvascular remodeling, normoxygenation, and cell proliferation in portal blood-deprived liver tissue

Cited by 52 publications

References 33 publications

Portal Cavernoma Cholangiopathy: Consensus Statement of a Working Party of the Indian National Association for Study of the Liver

Portal Cavernoma Cholangiopathy: Consensus Statement of a Working Party of the Indian National Association for Study of the Liver

Induction of Tumor Growth After Preoperative Portal Vein Embolization: Is It a Real Problem?

Hepatic Arterial Infusion with Tumor Necrosis Factor-α Induces Early Hepatic Hyperperfusion

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