Impairment of chronotropic response to the β-agonist isoproterenol in rats with portal hypertension due to portal vein stenosis or bile-duct ligation

1985 ◽  
Vol 1 ◽  
pp. S59 ◽  
Keyword(s):  
Portal Hypertension ◽  
Bile Duct ◽  
Portal Vein ◽  
Bile Duct Ligation ◽  
Chronotropic Response ◽  
Portal Vein Stenosis ◽  
Duct Ligation ◽  
Vein Stenosis

Effect of Two Models of Portal Hypertension on Splanchnic Organ Blood Flow in the Rat

1985 ◽  
Vol 68 (1) ◽  
pp. 23-28 ◽  
Author(s):  
D. Lebrec ◽  
L. Blanchet
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Portal Hypertension ◽  
Portal Vein ◽  
Arterial Blood Flow ◽  
Organ Blood Flow ◽  
Portal Vein Stenosis ◽  
Arterial Blood ◽  
Duct Ligation ◽  
Vein Stenosis

1. Splanchnic organ blood flow and cardiac output were measured by the microsphere method in fasted rats with prehepatic portal hypertension due to portal vein stenosis, in rats with intrahepatic portal hypertension due to bile duct ligation, and in unoperated normal rats. 2. Portal venous pressure was higher in both groups of portal hypertensive rats than in normal rats. Cardiac output was significantly higher in portal hypertensive rats than in normal rats. 3. In rats with portal vein stenosis, splanchnic blood flow was higher than in controls. This increase was caused by increased perfusion of all organs drained by the portal vein, and by increased hepatic arterial blood flow. In rats with bile duct ligation, splanchnic blood flow was not significantly higher than in normal rats: haemoperfusion of all organs contributing to the portal circulation decreased, whereas hepatic arterial blood flow increased. As cardiac output rose similarly, the differences observed between the two types of portal hypertension depend mainly on the difference in distribution of flow within the splanchnic bed.

scholarly journals Correction of extrahepatic portal hypertension in pediatric patient after liver transplantation

2017 ◽  
Vol 19 (1) ◽  
pp. 47-51
Author(s):  
A. R. Monakhov ◽  
B. L. Mironkov ◽  
T. A. Dzhanbekov ◽  
K. O. Semash ◽  
Kh. M. Khizroev ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Blood Flow ◽  
Portal Hypertension ◽  
Portal Vein ◽  
Pediatric Patient ◽  
Portal Blood Flow ◽  
Portal Blood ◽  
Positive Trend ◽  
Portal Vein Stenosis ◽  
Vein Stenosis

Introduction. Liver transplantation is a multi-component and complex type of operative treatment. Patients undergoing such a treatment sometimes are getting various complications. One of these complications is a portal hypertension associated with portal vein stenosis.Materials and methods. In 6 years after the left lateral section transplantation from living donor in a pediatric patient the signs of portal hypertension were observed. Stenosis of the portal vein was revealed. Due to this fact percutaneous transhepatic correction of portal vein stenosis was performed.Results. As a result of the correction of portal blood flow in the patient a positive trend was noted. According to the laboratory and instrumental methods of examination the graft had a normal function, portal blood flow was adequate. In order to control the stent patency Doppler ultrasound and MSCT of the abdominal cavity with intravenous bolus contrasting were performed. Due to these examinations the stent function was good, the rate of blood flow in the portal vein due to Doppler data has reached 80 cm/sec, and a decrease of the spleen size was noted.Conclusion. Diagnosis and timely detection of portal vein stenosis in patients after liver transplantation are very important for the preservation of graft function and for the prevention of portal hypertension. In order to do that, ultrasound Doppler fluorimetry examination needs to be performed to each patient after liver transplantation. In cases of violation of the blood flow in the portal vein CT angiography performance is needed. Percutaneous transhepatic stenting of portal vein is a minimally invasive and highly effective method of correction of portal hypertension. Antiplatelet therapy and platelet aggregation control are the prerequisites for successful stent function.

Electroacupuncture attenuates vascular hyporeactivity in a rat model of portal hypertension induced by bile duct ligation

2021 ◽  
pp. 096452842110392
Author(s):  
Yu-Sheng Chen ◽  
Chorng-Kai Wen ◽  
Geng-Hao Liu ◽  
Tzung-Yan Lee
Keyword(s):  
Portal Hypertension ◽  
Growth Factor ◽  
Bile Duct ◽  
Bile Duct Ligation ◽  
Portal Pressure ◽  
Contractile Responses ◽  
Hyperdynamic Circulation ◽  
Duct Ligation ◽  
Tnf Α ◽  
Cox 1

Background: A hyperdynamic circulation and impaired vascular responsiveness to vasoconstrictors are observed in portal hypertension (PHT) rats. Inflammation is a major contributor to the hyperdynamic circulation state in murine models of PHT. Electroacupuncture (EA) may ameliorate the inflammatory response and limit arterial vasodilatation and portal pressure. This study investigated the possible mechanisms underlying putative hemodynamics effects of EA in normal and PHT rats. Methods: PHT was induced by bile duct ligation (BDL) surgery over 4 weeks in rats. Sham-operated and BDL rats were treated with low-frequency EA (2 Hz) at ST36 10 min three times weekly for one or two consecutive weeks (for a total of 3 or 7 treatments, respectively). Serum tumor necrosis factor-α (TNF-α), nitrite/nitrate (NOx) and 6-keto-prostaglandin F1α (6-keto-PGF1α) were analyzed, and hemodynamic variation and contractile responses to phorbol-12,13-dibutyrate and phenylephrine in aortic and superior mesenteric arterial rings were recorded. Inducible (i) and endothelial (3) nitric oxide synthase (NOS), cyclooxygenase-1 (COX-1), and protein kinase C-α (PKC-α) levels were determined by Western blotting. Results: EA significantly reduced portal pressure and serum TNF-α, NOx and 6-keto-PGF1α levels compared to the untreated BDL group, enhanced maximum contractile responses in the aorta, up-regulated PKC-α, and down-regulated iNOS and COX-1 levels. In addition, EA decreased the aortic angiogenesis signaling cascade, reflected by down-regulation of vascular endothelial growth factor (VEGF) abundance and transforming growth factor β receptor (TGFβR)I/II expression, as assessed by immunostaining. Conclusion: EA attenuates TNF-α, NO and 6-keto-PGF1α overproduction, modulates the vascular levels of constitutive NOS and PKC-α, blunts the development of the angiogenesis cascade, and enhances vascular contractile force in PHT rats.

Common bile duct ligation in the rat: a model of intrapulmonary vasodilatation and hepatopulmonary syndrome

1997 ◽  
Vol 272 (4) ◽  
pp. G779-G784 ◽  
Author(s):  
M. B. Fallon ◽  
G. A. Abrams ◽  
J. W. McGrath ◽  
Z. Hou ◽  
B. Luo
Keyword(s):  
Portal Hypertension ◽  
Bile Duct ◽  
Gas Exchange ◽  
Common Bile Duct ◽  
Lung Injury ◽  
Bile Duct Ligation ◽  
Hepatopulmonary Syndrome ◽  
Common Bile Duct Ligation ◽  
Arterial Blood ◽  
Duct Ligation

Hepatopulmonary syndrome (HPS) causes impaired oxygenation due to intrapulmonary vasodilatation in patients with cirrhosis. Chronic common bile duct ligation (CBDL) in the rat results in gas-exchange abnormalities similar to HPS, but intrapulmonary vasodilatation has not been evaluated. We assess intrapulmonary vasodilatation, measured in vivo, after CBDL. Sham, 2- and 5-wk CBDL, and 3-wk partial portal vein ligated (PVL) rats had hepatic and lung injury, portal pressure, and arterial blood gases assessed. The pulmonary microcirculation was evaluated by injecting microspheres (size range 5.5-10 microm) intravenously and measuring the size and number of microspheres bypassing the lungs in arterial blood. CBDL animals developed progressive hepatic injury and portal hypertension accompanied by gas-exchange abnormalities and intrapulmonary vasodilatation. PVL animals, with a similar degree of portal hypertension, did not develop intrapulmonary vasodilatation or abnormal gas exchange. No lung injury was observed. CBDL, but not PVL, causes progressive intrapulmonary vasodilatation, which accompanies worsening arterial gas exchange. These findings validate CBDL as a model to study HPS.

Evaluation of bile duct ligation-induced portal vein hypertension in telemetered rats

2013 ◽  
Vol 68 (1) ◽  
pp. e45
Author(s):  
Philippe Guillaume ◽  
David Virley ◽  
Sylvie Bézivin ◽  
Sonia Rompion ◽  
Guillaume Froget
Keyword(s):  
Bile Duct ◽  
Portal Vein ◽  
Bile Duct Ligation ◽  
Portal Vein Hypertension ◽  
Duct Ligation

Early colchicine administration reduces hepatic fibrosis and portal hypertension in rats with bile duct ligation

1993 ◽  
Vol 19 (1) ◽  
pp. 90-94 ◽  
Author(s):  
Jorge L. Poo ◽  
Gérard Feldmann ◽  
Alain Moreau ◽  
Christophe Gaudin ◽  
Didier Lebrec
Keyword(s):  
Portal Hypertension ◽  
Bile Duct ◽  
Hepatic Fibrosis ◽  
Bile Duct Ligation ◽  
Duct Ligation

Renal perfusion in dogs with experimental hepatic cirrhosis: role of prostaglandins

1983 ◽  
Vol 245 (4) ◽  
pp. F521-F529
Author(s):  
M. Levy ◽  
M. J. Wexler ◽  
C. Fechner
Keyword(s):  
Portal Hypertension ◽  
Bile Duct ◽  
Bile Duct Ligation ◽  
Renin Angiotensin System ◽  
Renal Perfusion ◽  
Venous Hypertension ◽  
Prostaglandin Synthesis ◽  
Portacaval Anastomosis ◽  
Duct Ligation ◽  
Pah Clearance

Increased renal production of prostaglandins are thought to be important for the maintenance of kidney blood flow in advanced cirrhosis. In alert, unanesthetized dogs with chronic cirrhosis and ascites, produced by bile duct ligation, we measured inulin and p-aminohippurate (PAH) clearance before and after the intravenous administration of 2 mg/kg indomethacin, an inhibitor of prostaglandin production. Inulin and PAH clearance declined by 42 and 43%, respectively. This decline in renal perfusion was not associated with changes in blood pressure or cardiac output. If portal hypertension was prevented by creating an end-side portacaval anastomosis at the time of bile duct ligation, indomethacin was without effect on renal perfusion whether or not the dog had ascites. If ascites was completely mobilized in cirrhotic dogs with portal venous hypertension with the aid of a LeVeen valve, indomethacin depressed inulin and PAH clearance as usual during the steady-state period once all ascites had been removed. An attempt was made to determine some of the factors mediating the apparent increase in renal prostaglandin synthesis by administering various pharmacological antagonists. The inhibition of angiotensin effect with saralasin and the inhibition of kallikrein with aprotinin prevented the usual indomethacin effect. It is concluded that portal hypertension, but not a “sick liver per se, in cirrhosis activates the renin-angiotensin system to both produce renal vasoconstriction and stimulate prostaglandin synthesis, thereby normalizing renal perfusion. Renal kallikrein also appears to play a role, probably by augmenting renin release.

Effects of simvastatin, pentoxifylline and spironolactone on hepatic fibrosis and portal hypertension in rats with bile duct ligation

1997 ◽  
Vol 26 (6) ◽  
pp. 1363-1371 ◽  
Author(s):  
Frédéric Oberti ◽  
Christophe Pilette ◽  
Hervé Rifflet ◽  
Moussa Y. Maïga ◽  
Alain Moreau ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Bile Duct ◽  
Hepatic Fibrosis ◽  
Bile Duct Ligation ◽  
Duct Ligation

Prevention of portal hypertension by propanolol and spironolactone in rats with bile duct ligation

1997 ◽  
Vol 26 (1) ◽  
pp. 167-173 ◽  
Author(s):  
Frédéric Oberti ◽  
Hervé Rifflet ◽  
Moussa Y. Maïga ◽  
Christophe Pilette ◽  
Yves Gallois ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Bile Duct ◽  
Bile Duct Ligation ◽  
Duct Ligation
Sign in / Sign up

Export Citation Format

Share Document