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

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.

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

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1985.249.4.g528 ◽

1985 ◽

Vol 249 (4) ◽

pp. G528-G532 ◽

Cited By ~ 6

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.

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Correction of extrahepatic portal hypertension in pediatric patient after liver transplantation

Russian Journal of Transplantology and Artificial Organs ◽

10.15825/1995-1191-2017-1-47-51 ◽

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.

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Abstract 67: Vasopressin impairs Brain, Heart and Kidney Perfusion in Acute Heart Failure

Circulation ◽

10.1161/circ.116.suppl_16.ii_937-b ◽

2007 ◽

Vol 116 (suppl_16) ◽

Author(s):

Stig Müller ◽

Ole-Jakob How ◽

Stig E Hermansen ◽

Truls Myrmel

Keyword(s):

Blood Flow ◽

Cardiac Output ◽

Heart Function ◽

Left Ventricular Pressure ◽

Left Ventricular ◽

Arterial Blood Flow ◽

Organ Blood Flow ◽

Arterial Blood ◽

Time Flow ◽

The Brain

Arginin Vasopressin (AVP) is increasingly used to restore mean arterial pressure (MAP) in various circulatory shock states including cardiogenic shock. This is potentially deleterious since AVP is also known to reduce cardiac output by increasing vascular resistance. Aim: We hypothesized that restoring MAP by AVP improves vital organ blood flow in experimental acute cardiac failure. Methods: Cardiac output (CO) and arterial blood flow to the brain, heart, kidney and liver were measured in nine pigs by transit-time flow probes. Heart function and contractility were measured using left ventricular Pressure-Volume catheters. Catheters in central arteries and veins were used for pressure recordings and blood sampling. Left ventricular dysfunction was induced by intermittent coronary occlusions, inducing an 18 % reduction in cardiac output and a drop in MAP from 87 ± 3 to 67 ± 4 mmHg. Results: A low-dose therapeutic infusion of AVP (0.005 u/kg/min) restored MAP but further impaired systemic perfusion (CO and blood flow to the brain, heart and kidney reduced by 29, 18, 23 and 34 %, respectively). The reduced blood flow was due to a 2.0, 2.2, 1.9 and 2.1 fold increase in systemic, brain, heart and kidney specific vascular resistances, respectively. Contractility remained unaffected by AVP. The hypoperfusion induced by AVP was most likely responsible for observed elevated plasma lactate levels and an increased systemic oxygen extraction. Oxygen saturation in blood drawn from the great cardiac vein fell from 31 ± 1 to 22 ± 3 % dropping as low as 10 % in one pig. Finally, these effects were reversed forty minutes after weaning the pigs form the drug. Conclusion: The pronounced reduction in coronary blood flow point to a potentially deleterious effect in postoperative cardiac surgical patients and in patients with coronary heart disease. Also, this is the first study to report a reduced cerebral perfusion by AVP.

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Role of glucagon in splanchnic hyperemia of chronic portal hypertension

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1986.251.5.g674 ◽

1986 ◽

Vol 251 (5) ◽

pp. G674-G677 ◽

Cited By ~ 7

Author(s):

J. N. Benoit ◽

B. Zimmerman ◽

A. J. Premen ◽

V. L. Go ◽

D. N. Granger

Keyword(s):

Blood Flow ◽

Portal Hypertension ◽

Venous Blood ◽

Reference Sample ◽

Venous Hypertension ◽

Arterial Blood Flow ◽

Venous Blood Flow ◽

Portal Vein Stenosis ◽

Arterial Blood

The role of glucagon as a blood-borne mediator of the hyperdynamic circulation associated with chronic portal venous hypertension was assessed in the rat portal vein stenosis model. Selective removal of pancreatic glucagon from the circulation was achieved by intravenous infusion of a highly specific glucagon antiserum. Blood flow to splanchnic organs, kidneys, and testicles was measured with radioactive microspheres, and the reference-sample method. Glucagon antiserum had no effect on blood flow in the gastrointestinal tract of sham-operated (control) rats. However, the antiserum produced a significant reduction in hepatic arterial blood flow in the control rats, suggesting that glucagon contributes significantly to the basal tone of hepatic arterioles. In portal hypertensive rats glucagon antiserum significantly reduced blood flow to the stomach (22%), duodenum (25%), jejunum (24%), ileum (26%), cecum (27%), and colon (26%). Portal venous blood flow was reduced by approximately 30%. The results of this study support the hypothesis that glucagon mediates a portion of the splanchnic hyperemia associated with chronic portal hypertension.

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Cardiac output and redistribution of organ blood flow in hypermetabolic sepsis

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1984.246.3.r331 ◽

1984 ◽

Vol 246 (3) ◽

pp. R331-R337 ◽

Cited By ~ 8

Author(s):

C. H. Lang ◽

G. J. Bagby ◽

J. L. Ferguson ◽

J. J. Spitzer

Keyword(s):

Blood Flow ◽

Cardiac Output ◽

Muscle Blood Flow ◽

Intraperitoneal Administration ◽

Peripheral Resistance ◽

Arterial Blood Flow ◽

Tissue Blood Flow ◽

Organ Blood Flow ◽

Arterial Blood ◽

Over Time

Cardiac output (CO) and the distribution of blood flow were studied in chronically catheterized conscious rats during sustained (4 days) sepsis. Septicemia was induced by intraperitoneal administration of a pooled fecal inoculum, and tissue blood flow and CO were determined daily with 15-micron radioactive microspheres. Mean arterial blood pressure (MABP, 113 +/- 2 mmHg), CO (244.5 +/- 11.4 ml X min-1 X kg-1), and total peripheral resistance (TPR, 1.36 +/- 0.07 mmHg X ml-1 X min) were stable in control rats over the 4 days postinoculation. Septic animals showed a consistent tachycardia with MABP significantly reduced only on days 3 and 4 (86 +/- 4 mmHg). A hyperdynamic response to sepsis was indicated by an elevated CO (27%) and similarly reduced TPR on day 2. The calculated stroke volume averaged 0.22 +/- 0.01 ml/beat and did not vary over time or between the two groups. There was a 40-70% increase in blood flow to the heart, spleen, adrenal glands, and small intestine, and a greater than sixfold increase in hepatic arterial blood flow. The sustained elevation of coronary blood flow, observed in septic animals, was independent of myocardial work and is consistent with impaired myocardial function. Pancreas, stomach, and skeletal muscle blood flow was consistently compromised (24, 39, and 52%, respectively) during sepsis. Blood flow in other organs remained unchanged over time. Sepsis-induced changes in the fractional distribution of blood flow to various organs were similar to those described for absolute flow. (ABSTRACT TRUNCATED AT 250 WORDS)

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Assessment of hemodynamic parameters of hepatic and visceral blood flow in decompensated liver cirrhosis

Zaporozhye Medical Journal ◽

10.14739/2310-1210.2021.3.224265 ◽

2021 ◽

Vol 23 (3) ◽

pp. 363-369

Author(s):

A. S. Tugushev ◽

O. S. Cherkovska ◽

D. I. Mikhantiev

Keyword(s):

Blood Flow ◽

Liver Cirrhosis ◽

Portal Hypertension ◽

Portal Vein ◽

Hepatic Blood Flow ◽

Natural Course ◽

Arterial Blood Flow ◽

Hemodynamic Parameters ◽

Decompensated Liver Cirrhosis ◽

Arterial Blood

The aim. To assess the hemodynamic parameters of the hepatic and visceral blood flow in patients with compensated and decompensated liver cirrhosis. Materials and methods. 290 patients with liver cirrhosis were examined: 206 had gastrointestinal bleeding, 84 had diuretic-resistant ascites. Ultrasonic scanning, Doppler sonography, esophagogastroduodenoscopy, angiography, radioisotope scintigraphy were performed to assess blood flow in the portal, splenic and superior mesenteric veins and in the hepatic, splenic and superior mesenteric arteries. Results. Change in the hepatic microcirculatory blood flow in the natural course of liver cirrhosis was characterized by decreased portal and increased arterial blood flow, “arterialization” of hepatic blood flow based on scintigraphy. Decompensation of the disease was associated with progressive reduction in both portal and arterial hepatic blood flow, which were correlated with the severity of functional liver disorders regardless of the complication nature. The portal blood flow in the natural course of liver cirrhosis was characterized by 3.5–4.5 times increased volume of visceral blood. Decompensation of the disease was accompanied by a decrease in blood flow in the portal vein as compared to the splenic and superior mesenteric veins by 1.8–2.2 and 1.5–2.7 times, respectively. Arterial blood flow in the natural course of liver cirrhosis was characterized by a relatively increased hepatic arterial flow. The ultrasound criterion of hepatic blood flow “arterialization” was an increase in hepatic-splenic arterial index, which can be used as a sign to differentiate between different forms of portal hypertension. Decompensation of the disease was characterized by an average of 8.2 % decreased arterial blood flow in the hepatic artery compared to the splenic artery in dynamics. Prognostically unfavorable signs were the progression of splenomegaly degree, the increase in the portal vein diameter with the decreased velocity characterizing the increase in congestive index by 2.4–2.6 times, the decrease in the hepatic artery diameter and velocity in it over time.Conclusions. The hepatic and visceral blood flow characteristics should be considered when choosing method of conservative, surgical or minimally invasive treatment of liver cirrhosis complications. Based on the hepatic hemodynamic characteristics, the mismatch between portal perfusion (reduced) and visceral blood flow (increased) is the essence of portal hypertension in liver cirrhosis. Accordingly, the criterion of treatment effectiveness in decompensated liver cirrhosis should be improved portal liver perfusion and (or) reduced volume of visceral blood flow.

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

Clinical Science ◽

10.1042/cs0630029 ◽

1982 ◽

Vol 63 (1) ◽

pp. 29-32 ◽

Cited By ~ 38

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.

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