Free and conjugated plasma catecholamines in normal rats and in rats with portal hypertension due to portal vein stenosis

1985 ◽  
Vol 1 ◽  
pp. S238
Author(s):  
A. R. Monakhov ◽  
B. L. Mironkov ◽  
T. A. Dzhanbekov ◽  
K. O. Semash ◽  
Kh. M. Khizroev ◽  
...  

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.


2011 ◽  
Vol 62 (1) ◽  
pp. 245-255 ◽  
Author(s):  
Dexin Lin ◽  
Xianbin Wu ◽  
Xiaoke Ji ◽  
Qiyu Zhang ◽  
YuanWei Lin ◽  
...  

1998 ◽  
Vol 94 (6) ◽  
pp. 645-650 ◽  
Author(s):  
Han-Chieh Lin ◽  
Yi-Tsau Huang ◽  
Yuh-Ren Cheng ◽  
Ming-Chih Hou ◽  
Fa-Yauh Lee ◽  
...  

1. Both octreotide and isosorbide dinitrate have been shown to have portal hypotensive effects in animals with portal hypertension. Moreover, in both animals and humans with portal hypertension, the reduction of portal pressure was enhanced when nitrovasodilators were combined with propranolol or vasopressin. The present study was undertaken to evaluate the effect of long-term administration of octreotide and isosorbide dinitrate on haemodynamics in rats with portal vein stenosis. 2. Portal hypertension was induced by portal vein stenosis. Portal hypertensive rats were allocated into one of four groups (eight rats in each group): vehicle group, octreotide group (100 μg/kg via subcutaneous injection every 12 h), isosorbide dinitrate group (5 mg/kg via gastric gavage every 12 h) and combined treatment group. Drug was given for eight consecutive days, starting 1 day before surgery. Haemodynamic values were measured using a radioactive microsphere technique. 3. Long-term octreotide treatment decreased portal pressure and improved the hyperdynamic circulation. In contrast, long-term administration of isosorbide dinitrate reduced portal pressure but did not ameliorate vasodilatation. A combination of octreotide and isosorbide dinitrate improved the hyperdynamic circulation with a reduction of portal pressure. In addition, the mean value of portal pressure after combination treatment was significantly lower than in rats receiving octreotide alone. 4. These results showed that, in rats with portal hypertension, long-term combined administration of octreotide and isosorbide dinitrate improved the hyperdynamic circulation together with a more profound reduction of portal pressure than rats receiving octreotide alone.


1985 ◽  
Vol 249 (4) ◽  
pp. G528-G532 ◽  
Author(s):  
S. S. Lee ◽  
C. Girod ◽  
D. Valla ◽  
P. Geoffroy ◽  
D. Lebrec

To determine the effect of pentobarbital sodium anesthesia on the rat with portal hypertension due to portal vein stenosis, four groups of rats were studied. Cardiac output and regional blood flow were measured by radioactive microspheres in anesthetized and conscious sham-operated and portal-hypertensive rats. Anesthesia markedly decreased cardiac output in both sham-operated (109.7 +/- 4.6 vs. 77.8 +/- 1.4 ml/min, P less than 0.001) and portal-hypertensive rats (130.1 +/- 7.6 vs. 93.8 +/- 5.3 ml/min, P less than 0.01). In spite of this diminution in cardiac output, pentobarbital did not significantly change absolute blood flow values of splanchnic organs in either group. However, the fractions of cardiac output perfusing the splanchnic organs were significantly increased by pentobarbital in both groups because of the decrease in cardiac output: sham operated, anesthetized, 22.86 +/- 1.19% vs. conscious, 14.83 +/- 1.02%, P less than 0.001; and portal hypertensive, anesthetized, 26.67 +/- 0.71% vs. conscious, 19.07 +/- 1.44%, P less than 0.001. The hyperdynamic circulation of the portal vein-stenosed rat compared with the sham-operated rat continued to manifest itself with significantly increased portal pressure, cardiac output, and splanchnic blood flow, whether the animal was anesthetized or awake. We conclude that, despite marked hemodynamic changes induced by pentobarbital, the rat with portal vein stenosis remains a useful experimental model of portal hypertension.


HPB Surgery ◽  
1998 ◽  
Vol 10 (6) ◽  
pp. 357-364 ◽  
Author(s):  
B. Malassagne ◽  
O. Soubrane ◽  
B. Dousset ◽  
P. Legmann ◽  
D. Houssin

This study reports our experience of 8 cases of extrahepatic portal hypertension after 273 orthotopic liver transplantations in 244 adult patients over a 10- year period. The main clinical feature was ascites, and the life-threatening complication was variceal bleeding. Extrahepatic portal hypertension was caused by portal vein stenosis in 6 patients, and left-sided portal hypertension in 2 patients after inadventent ligation of portal venous tributaries or portasystemic shunts. All patients with portal vein stenosis had complete relief of portal hypertension after percutaneous transhepatic venoplasty (n=4) or surgical reconstruction (n=2), after a median follow-up of 33 (range: 6–62) months. Of the 2 patients with left-sided portal hypertension, one died after splenectomy and one rebled 6 months after left colectomy. This study suggests that extrahepatic portal hypertension is a series complication after liver transplantation that could be prevented by meticulous portal anastomosis and closure of portal tributaries or portasystemic shunts to improve the portal venous flow. However, any ligation has to be performed under ultrasound guidance to avoid inadventent venous ligations.


1985 ◽  
Vol 68 (1) ◽  
pp. 23-28 ◽  
Author(s):  
D. Lebrec ◽  
L. Blanchet

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.


1985 ◽  
Vol 248 (2) ◽  
pp. G192-G195 ◽  
Author(s):  
J. W. Kiel ◽  
V. Pitts ◽  
J. N. Benoit ◽  
D. N. Granger ◽  
A. P. Shepherd

The development of portal hypertension following chronic portal vein stenosis is accompanied by a significant increase in intestinal blood flow. The present study was designed to determine whether intestinal vascular sensitivity to norepinephrine (NE) is also affected by chronic portal vein stenosis. Using a blood-perfused, in situ rat small intestine preparation, we found that, when compared with control animals, a significantly greater molar concentration of NE was required to achieve the same proportional increase in intestinal vascular resistance in portal-hypertensive animals. The mean ED50 value (+/-SE) for the portal-hypertensive group (704.3 +/- 186.1 nM) was significantly greater (P less than 0.05) than the mean ED50 value for the control group (271.4 + 48.1 nM). This finding implies that sympathetic maintenance of intestinal vascular tone may be impaired following chronic portal vein stenosis, possibly accounting for part of the intestinal hyperemia associated with portal hypertension.


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