Effect of Propranolol on Hepatic Blood Flow in Normal and Portal Hypertensive Rats

1982 ◽  
Vol 63 (1) ◽  
pp. 29-32 ◽  
Author(s):  
P. Hillon ◽  
L. Blanchet ◽  
D. Lebrec
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Portal Vein ◽  
Hepatic Artery ◽  
Hepatic Blood Flow ◽  
Venous Pressure ◽  
Portal Venous Pressure ◽  
Portal Vein Stenosis ◽  
Vein Stenosis

1. The effects of propranolol on heart rate, arterial pressure, portal venous pressure and fractional hepatic blood flow were studied in rats with hepatic artery ligature or with portal vein stenosis, and in sham-operated rats. The effect of propranolol on cardiac output was also studied in normal rats. 2. In rats with hepatic artery ligature or with portal vein stenosis, and in sham-operated rats, propranolol decreased heart rate and portal venous pressure significantly and did not alter arterial pressure. Propranolol decreased fractional hepatic blood flow significantly in rats with hepatic artery ligature, but did not change hepatic blood flow in rats with portal vein stenosis or in sham-operated rats. 3. We conclude therefore that: (a) propranolol decreases portal venous pressure in rats; (b) this decrease in portal venous pressure results in a reduction in portal blood flow which is related, in part, to a reduction in cardiac output; (c) propranolol does not alter hepatic blood flow in normal rats or in rats with portal hypertension.

Effects of pentobarbital sodium anesthesia on splanchnic hemodynamics of normal and portal-hypertensive rats

1985 ◽  
Vol 249 (4) ◽  
pp. G528-G532 ◽  
Author(s):  
S. S. Lee ◽  
C. Girod ◽  
D. Valla ◽  
P. Geoffroy ◽  
D. Lebrec
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Portal Hypertension ◽  
Portal Vein ◽  
Regional Blood Flow ◽  
Hypertensive Rats ◽  
Pentobarbital Sodium ◽  
Portal Vein Stenosis ◽  
Pentobarbital Sodium Anesthesia ◽  
Vein Stenosis

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.

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.

Effect of portal hypertension on splenic blood flow, intrasplenic extravasation and systemic blood pressure

2003 ◽  
Vol 284 (6) ◽  
pp. R1580-R1585 ◽  
Author(s):  
Susan Kaufman ◽  
Jody Levasseur
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Portal Hypertension ◽  
Portal Vein ◽  
Venous Pressure ◽  
Splenic Vein ◽  
Systemic Blood Pressure ◽  
Portal Venous Pressure ◽  
Systemic Blood ◽  
Fluid Extravasation

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.

Endovascular stenting of mesenterico-portal vein stenosis to reduce blood flow through venous collaterals prior to pancreatoduodenectomy

2015 ◽  
Vol 400 (5) ◽  
pp. 629-631 ◽  
Author(s):  
Terence C. Chua ◽  
Frank Wang ◽  
Richard Maher ◽  
Sivakumar Gananadha ◽  
Anubhav Mittal ◽  
...  
Keyword(s):  
Blood Flow ◽  
Portal Vein ◽  
Endovascular Stenting ◽  
Reduce Blood Flow ◽  
Portal Vein Stenosis ◽  
Venous Collaterals ◽  
Flow Through ◽  
Vein Stenosis

Changes Porto-hepatic Blood Flow in Patients with Cirrhosis of the Liver, Combined with Chronic Bronchitis

2016 ◽  
pp. 129-132
Author(s):  
Nataliia Virstyuk ◽  
Iryna Kobitovych ◽  
Olha Gerasymchuk
Keyword(s):  
Blood Flow ◽  
Portal Vein ◽  
Chronic Bronchitis ◽  
Hepatic Artery ◽  
Hepatic Blood Flow ◽  
Blood Flow Velocity ◽  
Splenic Artery ◽  
Splenic Vein ◽  
Resistance Index ◽  
Healthy Individuals

The objective: study the features of porto1hepatic blood flow in patients with alcoholic liver cirrhosis (ALC) in conjunction with chronic bronchitis (CB) according to Doppler ultrasound. Patients and methods. The study involved 60 patients who were hospitalized, 20 ALC patients in stage B according to Child-Pugh without CB (Ist group), 20 ALC patients in stage B according to Child-Pugh combined with CB in the acute phase (IInd group), 20 patients exacerbation of chronic bronchitis, for which there was no evidence of digestive system diseases (IIIrd group). All patients underwent a complex ultrasonic research techniques scanning in B-mode, the VD-mode, color duplex scanning using «Hitachi EUB 7000» ultrasonic scanner connected to the Doppler flourimetr was visualized main arterial and venous vessels of hepatic and splenic pools. Results. Changes porto-hepatic blood flow were most pronounced in patients with ALC in combination with CB when compared with patients of groups I and III (p<0,05) according to the obtained Doppler indices: diameter of the hepatic artery was 5,55±0,19 mm, portal vein – 12,60±0,17 mm, where increased by 159,12% and 53,56%, respectively (p<0,05) higher than those in healthy individuals. The diameter of the splenic artery and splenic vein at the ALC for combination with CB significantly increased compared with control on 31,13% and 35,67%, respectively (p<0,05). Linear and volumetric blood flow rate in portal vein decreased in this group of patients, 60,24% and 22,68%, respectively (p<0,05) compared with healthy individuals, the linear velocity of blood flow in the splenic vein also significantly slowed down compared to the control on 41,06% (p<0,05), and the volumetric blood flow velocity v. lienalis grew by 155,80% (p<0,05). Among the characteristics of the arterial blood flow hepato-splenic system Gosling pulsatility index (PI) and Pursello resistance index (RI) of hepatic artery also Pursello resistance index (RI) of splenic artery significantly grew in ALC patients in combination with CB 147,20%, 65,49% and 32,31%, respectively (p<0,05) compared with the control group. Maximal systolic velocity of blood flow in the hepatic artery of patients – grew by 8,95% (p<0,05). End diastolic blood flow velocity in the hepatic artery tended to decrease on 13,36% (p<0,05) compared with healthy individuals. Conclusion. Violation of porto-hepatic blood flow in patients with ALC is characterized by its redistribution in the veins of the portal system in the direction of the spleen with a decrease in the average linear and the volumetric velocity in the portal and hepatic veins, increasing the resistance index in the interlobar arteries.

The Haemodynamic Effects of Metabolic Acidosis in the Rat

1976 ◽  
Vol 50 (3) ◽  
pp. 177-184 ◽  
Author(s):  
J. Yudkin ◽  
R. D. Cohen ◽  
Barbara Slack
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Metabolic Acidosis ◽  
Renal Blood Flow ◽  
Hepatic Blood Flow ◽  
Conscious Rats ◽  
Blood Ph ◽  
Significant Difference

1. The effect of metabolic acidosis of 4–6 h duration on cardiac output, blood pressure, heart rate, and hepatic and renal blood flow has been studied in the rat. 2. In anaesthetized rats, blood pressure and heart rate fell linearly with blood pH in both sham-operated and nephrectomized rats. There was no significant difference between the two groups in the effect of acidosis on either variable. 3. Cardiac output showed a significant fall with increasing acidosis in the conscious rat. 4. Estimated hepatic blood flow in conscious rats showed a significant positive correlation with blood pH in both sham-operated and nephrectomized animals. There was no significant difference in estimated hepatic blood flow between the two groups of animals at any blood pH. 5. In conscious rats, increasing acidosis caused a progressive decrease in estimated renal blood flow. 6. It is concluded that the increase in the previously described apparent renal contribution to lactate removal in the acidotic rat cannot be explained by any circulatory effect mediated by the kidney. The possible relevance of the findings to lactate homeostasis is discussed.

scholarly journals The relationship between intrahepatic portal systemic shunts and microsphere induced portal hypertension in the rat liver

Gut ◽  
1998 ◽  
Vol 42 (2) ◽  
pp. 276-282 ◽  
Author(s):  
X Li ◽  
I S Benjamin ◽  
B Alexander
Keyword(s):  
Blood Flow ◽  
Portal Hypertension ◽  
Steady State ◽  
Portal Vein ◽  
Rat Liver ◽  
Venous Pressure ◽  
Portal Venous Pressure ◽  
Portal Vein Ligation ◽  
The Relationship ◽  
Wedged Hepatic Venous Pressure

Background—Portal hypertension is associated with gross haemodynamic disturbances characterised by high cardiac output, low peripheral vascular resistance, increased splanchnic blood flow, and portal systemic shunting.Aims—To study the relationship between intrahepatic portal systemic shunts and microsphere induced portal hypertension in the rat liver.Methods—Different sized microspheres were sequentially injected into the portal vein of male Wistar rats.Results—Steady state portal venous pressure was increased by 102.2 (35.6)% (14.9 (3.6) mm Hg) and 272.3 (78.0)% (24.0 (2.2) mm Hg) above the basal pressure following sequential injections of 15 and 80 μm diameter microspheres, respectively. Sequential injection of 15, 40, and 80 μm diameter microspheres in either ascending or descending order of size did not generate further increases in portal venous pressure. A single injection of 1.8 × 105 80 μm microspheres consistently produced a steady state portal venous pressure of 19.0 (1.3) mm Hg but did not approach the much higher value of 36.6 (43.2) mm Hg measured during clamping of the portal vein. These data indicate that the opening of patent intrahepatic shunts was responsible for the reduced pressures observed during microsphere injections and further evidence for this was provided by the location of microspheres in the pulmonary vascular bed. The elevation in portal venous pressure achieved by microsphere injections was not significantly different to that produced in rats subjected to partial portal vein ligation (20.7 (0.5) mm Hg, p>0.05). Wedged hepatic venous pressure decreased from 6.7 (0.7) to 3.0 (0.6) mm Hg following injection of 80 μm microspheres, suggesting a decrease in total hepatic blood flow. Conversely, injection of 15 μm microspheres induced an increase in wedged hepatic venous pressure from 7.0 (1.0) mm Hg to 12.4 (1.8) mm Hg, indicating a localised redistribution of blood flow at the presinusoidal level of the portal venous vascular network and increased intrahepatic shunt flow.Conclusion—It is suggested that there may be a protective pathophysiological role for these shunts when the liver is subjected to changes which induce acute portal hypertension.

Hepatic vascular response to epinephrine

1961 ◽  
Vol 201 (1) ◽  
pp. 58-62 ◽  
Author(s):  
William C. Shoemaker ◽  
L. Newton Turk ◽  
Francis D. Moore
Keyword(s):  
Blood Flow ◽  
Portal Vein ◽  
Pressure Gradient ◽  
Hepatic Blood Flow ◽  
Femoral Vein ◽  
Venous Pressure ◽  
Portal Vein Pressure ◽  
Pronounced Increase ◽  
Epinephrine Administration ◽  
Arterial Blood

Hepatic hemodynamic events were measured before and after epinephrine administration in unanesthetized dogs in which the hepatic vessels had been previously catheterized. Comparisons were made of the response after a single intravenous injection at various doses and after a constant infusion of epinephrine; comparisons were also made between portal vein and femoral vein injections. After femoral venous injection of epinephrine (1–10 µg/kg) there was a marked increase in hepatic blood flow, roughly increasing with the size of the dose. With doses of 25 µg/kg or more, an initial increase in hepatic blood flow was followed by a decreased flow; in some instances death ensued. Epinephrine injected into the femoral vein produced a rise in the arterial blood pressure, followed by a rise in the portal vein pressure, portal-hepatic venous pressure gradient, and mechanical impedance across the hepatic venous bed. When injected into the portal vein under comparable conditions, epinephrine produced little or no change in hepatic blood flow or arterial pressure, but did produce a more rapid and pronounced increase in portal vein pressure, portal-hepatic pressure gradient and hepatic venous impedance.

Sign in / Sign up

Export Citation Format

Share Document