Hyperdynamic circulation in portal-hypertensive rat model: a primary factor for maintenance of chronic portal hypertension

1983 ◽  
Vol 244 (1) ◽  
pp. G52-G57 ◽  
Author(s):  
J. Vorobioff ◽  
J. E. Bredfeldt ◽  
R. J. Groszmann

Two dissimilar hemodynamic hypotheses, the “backward flow” theory and the “forward flow” theory, have been advanced to define splanchnic hemodynamics in portal hypertension. An animal model with portal hypertension and high-grade portal-systemic shunting, the portal vein-stenotic rat, was studied to determine whether a hemodynamic picture compatible with either theory would develop. Splanchnic and systemic hemodynamics and portal-systemic shunting were measured by radioactive microsphere techniques. The portal-hypertensive rats (portal pressure, 12.8 +/- 0.5 vs. 8.3 +/- 0.4 mmHg) with greater than 95% portal-systemic shunting had a 60% increase in portal venous inflow (23.46 +/- 2.54 vs. 14.97 +/- 1.61 ml/min; P less than 0.01) with a concomitant 50% decrease in splanchnic arteriolar resistance (3.86 +/- 0.43 vs. 7.60 +/- 0.80 dyn . s . cm-5 . 10(5); P less than 0.001) compared with control rats. Cardiac index (391 +/- 17 vs. 250 +/- 20 ml . min-1 . kg-1) was elevated 50% (P less than 0.001), and total peripheral resistance (7.1 +/- 0.4 vs. 11.7 +/- 0.8 dyn . s . cm-5 . 10(4)) was decreased 60% (P less than 0.001). The resistance to portal blood flow in portal vein-stenotic rats (4.77 +/- 0.57 dyn . s . cm-5 . 10(4)) was similar to the resistance to portal blood flow in control rats (4.82 +/- 0.43 dyn . s . cm-5 . 10(4)), indicating that the hyperdynamic portal venous inflow, not resistance, provided the main impetus for maintaining the elevated portal venous pressure. The splanchnic hemodynamic observations directly support the forward flow theory of portal hypertension. The relation between splanchnic arteriolar resistance and total peripheral resistance (r = 0.67; P less than 0.01) indicated that the systemic hemodynamic parameters were secondarily altered by the splanchnic hemodynamic changes. This animal model of chronic portal hypertension gave evidence for a generalized splanchnic arteriolar vasodilation occurring in the presence of high-grade portal-systemic shunting.

1986 ◽  
Vol 250 (2) ◽  
pp. G205-G212 ◽  
Author(s):  
E. Sikuler ◽  
R. J. Groszmann

To clarify the roles that portocollateral resistance ("backward-flow" theory) and portal flow ("forward-flow" theory) play in maintaining chronic portal hypertension, we studied, in a rat model with prehepatic portal hypertension, the hemodynamic changes that occur when portocollateral resistance is reduced and high portal venous inflow is maintained. In 30 portal-hypertensive rats the constriction around the portal vein was removed 4 days after induction of portal hypertension, 30 rats were used as portal vein-constricted controls, and 30 additional rats were subjected to a sham operation. The removal of the ligature constricting the portal vein was followed by an immediate decrease in portal pressure (from 16.3 +/- 0.8 to 9.6 +/- 0.8 mmHg, P less than 0.001). Two days after the ligature removal, hyperdynamic circulation was still evident and was characterized by a decreased splanchnic arteriolar resistance and an increased portal venous inflow. The coexistence of high portal venous inflow and normal portal pressure indicates that high portal venous inflow per se is not sufficient to produce an increase in portal pressure when it faces a low-resistance vascular bed. We conclude that portal hypertension is induced by the interaction of an abnormally high portal venous inflow and high resistance offered to the flow by the portocollateral vessels. Neither the forward-flow theory nor the backward-flow theory can be applied solely to explain the increased portal pressure.


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.


2016 ◽  
Vol 22 (2) ◽  
pp. 128-134 ◽  
Author(s):  
C. Anda Achim ◽  
P. Bordei ◽  
E. Dumitru

AbstractIntroduction: Portal hypertension results from increased resistance to the portal blood flow. The ultrasound represents a noninvasive tool for assessing the structural and hemodynamic abnormalities in this condition.Objectives: The assessment of the hemodynamic blood flow of the liver and spleen by using Doppler ultrasound in patients with portal hypertension compared with healthy subjects and to identify correlations with the severity of liver cirrhosis and esophageal varices.Materials and Method: This study included 50 patients with liver cirrhosis and 20 healthy subjects as controls. Different correlations were carried out between hemodynamic variables obtained from the Doppler examination and the severity of cirrhosis as assessed by the Child score and the degree of esophageal varices at endoscopy.Results: The portal vein diameter was larger in cirrhotic patients compared with the control group. The mean portal vein velocity and the blood flow were significantly lower in advanced forms of liver cirrhosis. The portal vein congestion index, the pulsatility and resistivity indexes of the hepatic artery were significantly increased in patients with CHILD B and C cirrhosis compared with the control group and patients in CHILD class A. There were no statistically significant differences between the pulsatility and resistivity indexes of the splenic artery in patients with cirrhosis. The liver vascular index was significantly lower in patients with advanced cirrhosis.Conclusions: The ultrasound is a valuable noninvasive tool for cirrhotic patients with portal hypertension. However, it is not sufficiently accurate in differentiating between different classes of cirrhosis or degrees of esophageal varices.


2017 ◽  
Vol 37 (10) ◽  
pp. 1172-1176 ◽  
Author(s):  
Alexandra F. Belotta ◽  
Bianca P. Santarosa ◽  
Danilo O.L. Ferreira ◽  
Sílvia M.F. Carvalho ◽  
Roberto C. Gonçalves ◽  
...  

ABSTRACT: Pulsed Doppler ultrasound was used to evaluate portal blood flow, portal velocity and portal congestion index in 24 healthy sheep divided into groups (lambs, yearlings and ewes), according to age. Measurements were performed at the 11th right intercostal space using ideal insonation angle and uniform insonation method. Mean values obtained in each group were compared with one-way ANOVA, followed by Tukey post-hoc test. Portal velocity and portal blood flow were statistically similar between the groups (P>0.05). Mean portal velocity were 17.75; 17.13 and 16.75; while mean portal blood flow were 26.65; 31.04 and 24.32 for lambs, yearlings and ewes, respectively. Portal congestion index was statistically distinct between the groups and values for lambs, yearlings and ewes were 0.009; 0.058 and 0.09, respectively (P<0.01). Statistical differences were observed in portal vein diameter, portal vein area and portal congestion index between the groups, presumably due to influence of weight and not to age.


2016 ◽  
Vol 2016 ◽  
pp. 1-5 ◽  
Author(s):  
Jiaxiang Meng ◽  
Qing Wang ◽  
Kai Liu ◽  
Shuofei Yang ◽  
Xinxin Fan ◽  
...  

Lipopolysaccharide (LPS) and endothelin- (ET-) 1 may aggravate portal hypertension by increasing intrahepatic resistance and splanchnic blood flow. In the portal vein, after TIPS shunting, LPS and ET-1 were significantly decreased. Our study suggests that TIPS can benefit cirrhotic patients not only in high hemodynamics related variceal bleeding but also in intestinal bacterial translocation associated complications such as endotoxemia.


2003 ◽  
Vol 284 (6) ◽  
pp. R1580-R1585 ◽  
Author(s):  
Susan Kaufman ◽  
Jody Levasseur

We have previously shown that intrasplenic fluid extravasation is important in controlling blood volume. We proposed that, because the splenic vein flows in the portal vein, portal hypertension would increase splenic venous pressure and thus increase intrasplenic microvascular pressure and fluid extravasation. Given that the rat spleen has no capacity to store/release blood, intrasplenic fluid extravasation can be estimated by measuring the difference between splenic arterial inflow and venous outflow. In anesthetized rats, partial ligation of the portal vein rostral to the junction with the splenic vein caused portal venous pressure to rise from 4.5 ± 0.5 to 12.0 ± 0.9 mmHg ( n = 6); there was no change in portal venous pressure downstream of the ligation, although blood flow in the liver fell. Splenic arterial flow did not change, but the arteriovenous flow differential increased from 0.8 ± 0.3 to 1.2 ± 0.1 ml/min ( n = 6), and splenic venous hematocrit rose. Mean arterial pressure fell (101 ± 5.5 to 95 ± 4 mmHg). Splenic afferent nerve activity increased (5.6 ± 0.9 to 16.2 ± 0.7 spikes/s, n = 5). Contrary to our hypothesis, partial ligation of the portal vein caudal to the junction with the splenic vein (same increase in portal venous pressure but no increase in splenic venous pressure) also caused the splenic arteriovenous flow differential to increase (0.6 ± 0.1 to 1.0 ± 0.2 ml/min; n = 8). The increase in intrasplenic fluid efflux and the fall in mean arterial pressure after rostral portal vein ligation were abolished by splenic denervation. We propose there to be an intestinal/hepatic/splenic reflex pathway, through which is mediated the changes in intrasplenic extravasation and systemic blood pressure observed during portal hypertension.


1992 ◽  
Vol 83 (1) ◽  
pp. 41-45 ◽  
Author(s):  
M. Dagenais ◽  
G. Pomier-Layrargues ◽  
B. Rocheleau ◽  
L. Giroux ◽  
P.-M. Huet

1. The systemic and splanchnic haemodynamic effects of pentifylline (40 mg/kg body weight intravenously) were assessed in rats with portal hypertension associated either with CCl4-induced cirrhosis (n= 13) or portal vein ligation (n=13). 2. Heparinized catheters were placed into the portal vein, inferior vena cava, aorta and left ventricle with exits from the neck. Haemodynamic studies were performed 4 h after consciousness was regained. Cardiac output and regional blood flows were measured using radiolabelled microspheres and the reference sample method in seven rats in each group; portal-systemic shunting was measured using microsphere injection in the ileo-colic vein in six rats in each group. 3. Forty-five minutes after injection, pentifylline had no effect on mean arterial pressure, cardiac output, peripheral resistance, portal venous flow, hepatic artery flow or portal-systemic shunting in either group of rats with portal hypertension. The drug lowered portal pressure (−18%) in cirrhotic rats, but not in portal-vein-ligated rats. 4. These data demonstrate that pentifylline lowers portal pressure in cirrhotic rats without affecting portal venous flow and portal-systemic shunting; this effect is possibly mediated by changes in intrahepatic resistance related to the effects of pentifylline on blood viscosity and/or on intrahepatic vasomotor tone.


HPB Surgery ◽  
1999 ◽  
Vol 11 (3) ◽  
pp. 151-155 ◽  
Author(s):  
Miguel Angel Mercado ◽  
Tito José María Gómez-Méndez ◽  
Julio César Morales-Linares ◽  
Jorge Granados ◽  
Carlos Chan ◽  
...  

Background; Surgery for portal hypertension has a low rebleeding rate. Patients that rebleed can be grossly divided into those who die as a consequence of the episode, those who don't die but develop liver failure (remaining as Child-Pugh C) and those who, in spite of the bleeding episode, retain good liver function (Child-Pugh A or B). At our hospital, the latter group is considered for further surgical treatment. We report here the results of surgical rescue of surgical failures.Methods; In a twenty year period, 36 patients (30 Child-Pugh A, 6 Child-Pugh B) were reoperated. The files of these patients were reviewed.Results; Average age was 33 years. Cirrhosis was present in 31 cases. All patients were electively reoperated with portal blood flow preserving procedures. Operative mortality for the whole group was 12% and for the Child-Pugh A group 6.6%. Rebleeding was observed in 5.5%. Postoperative incapacitating encephalopathy was recorded in one case (2.7%). Good quality of life was recorded in 84% of the cases. Survival (Kaplan-Meier) was 78% at 6 months and 69% at 5 years.Conclusions; Surgical failures in low risk patients (Child-Pugh A or B) can be treated by means of surgery, and a low mortality, re-bleeding and encephalopathy rate can be expected. The performance of a portal blood flow preserving procedure is recommended.


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