Background And Aim: Big animal models of portal hypertension are important for the research into this disease. The aim of this study was to establish a canine portal hypertension model by intra-portal administration of microspheres.
Methods: Sixteen mongrel dogs were assigned to control group and experimental group randomly. The catheterization of portal vein was performed by laparotomy and the outer end of the catheter was fixed subcutaneously in the abdominal wall. The dogs of the experimental group were given intra-portal injections of microspheres at a five-day interval, six times in total. Portal hemodynamics, blood cell counting, liver and renal function test, portography, gastroscopy, liver, spleen and lung histological examination were taken to evaluate the model.
Results: 1, 2, 3 and 4 months after initial injection of microspheres, portal venous pressure rose from baseline 8.7 +/- 0.7 mmHg to 24.3 +/- 1.6, 20.6 +/- 2.1, 19.0 +/- 1.8 and 17.7 +/- 2.0 mmHg, respectively (P < 0.01). The diameter of portal vein increased from 7.6 +/- 0.3 to 8.6 +/- 0.3 mm, calculated portal resistance increased from 0.46 +/- 0.06 to 1.06 +/- 0.20 (mmHg/mL/min/kg body weight); velocity of portal blood flow decreased from 35.1 +/- 1.7 to 26.1 +/- 2.4 cm/s (P < 0.01, respectively). The animals of experimental group developed marked splenomegaly and profuse portosystemic collateral circulations with normal liver and renal function.
Conclusion: Repeated intra-portal administration of microspheres can induce stable and reproducible chronic portal hypertension in dogs with normal liver and renal functions. This model can meet multiple demands of both basic and clinical research of portal hypertension.
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http://dx.doi.org/10.1111/j.1440-1746.2009.06158.x | DOI Listing |
HPB (Oxford)
January 2025
Hepato-Biliary Center, AP-HP Paul Brousse Hospital, Paris-Saclay University, INSERM Unit 1193, 94800 Villejuif, France. Electronic address:
Background: Liver cirrhosis accounts for more than 90 % of portal hypertension cases, and the other cases are due to noncirrhotic portal hypertension (NCPH). Variceal bleeding is the most life-threatening complication of portal hypertension and its primary treatment is medical according to the Baveno VII guidelines. This review discusses the evidence on surgical portal decompression for adult patients with NCPH secondary to chronic extrahepatic portal vein obstruction (EHPVO).
View Article and Find Full Text PDFPflugers Arch
January 2025
Leibniz Institute for Prevention Research and Epidemiology - BIPS, Bremen, Germany.
The global increase of overweight and obesity in children and adults is one of the most prominent public health threats, often accompanied by insulin resistance, hypertension, and dyslipidemia. The simultaneous occurrence of these health problems is referred to as metabolic syndrome. Various criteria have been proposed to define this syndrome, but no general consensus on the specific markers and the respective cut-offs has been achieved yet.
View Article and Find Full Text PDFLife (Basel)
January 2025
Department of Radiology, University Medical Center Regensburg, 93053 Regensburg, Germany.
Background: Portal vein thrombosis (PVT) leads to portal hypertension (PH) with its sequelae. Computed tomography spleno-mesenterico-portography (CT-SMPG) combines sequential CT spleno-portography and CT mesenterico-portography. CT-SMPG comprehensively illustrates the venous hemodynamic changes due to PH.
View Article and Find Full Text PDFMedicina (Kaunas)
December 2024
Clinic for Gastroenterology and Hepatology, University Clinical Centre of Serbia, 11 000 Belgrade, Serbia.
Cirrhotic cardiomyopathy (CCM) is a diagnostic entity defined as cardiac dysfunction (diastolic and/or systolic) in patients with liver cirrhosis, in the absence of overt cardiac disorder. Pathogenically, CCM stems from a combination of systemic and local hepatic factors that, through hemodynamic and neurohormonal changes, affect the balance of cardiac function and lead to its remodeling. Vascular changes in cirrhosis, mostly driven by portal hypertension, splanchnic vasodilatation, and increased cardiac output alongside maladaptively upregulated feedback systems, lead to fluid accumulation, venostasis, and cardiac dysfunction.
View Article and Find Full Text PDFAnn Med
December 2025
Department of Internal Medicine, Hallym Medical Center, Hallym University College of Medicine, Chuncheon, Republic of Korea.
Background/aims: Acute decompensation (AD) is defined as the development of complications related to portal hypertension and liver dysfunction that affect the progression of chronic liver disease (CLD) or liver cirrhosis (LC). Variations exist in patient demographics and prognostic outcomes of AD based on the aetiology of CLD, encompassing LC. However, limited research has been conducted to analyse these discrepancies across aetiologies.
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