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

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.

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.

General anesthesia and hepatic circulation

1987 ◽  
Vol 65 (8) ◽  
pp. 1762-1779 ◽  
Author(s):  
Simon Gelman
Keyword(s):  
Blood Flow ◽  
General Anesthesia ◽  
Surgical Procedures ◽  
Hepatic Blood Flow ◽  
Portal Blood Flow ◽  
Arterial Blood Flow ◽  
Hepatic Circulation ◽  
Arterial Blood ◽  
Total Hepatic Blood Flow ◽  
Circulatory Disturbances

This article describes hepatic circulatory disturbances associated with anesthesia and surgical intervention. The material is presented in three parts: part 1 describes the effects of general anesthetics on the hepatic circulation; part 2 deals with different factors related to surgical procedures and anesthesia; and part 3 analyzes the role of hepatic circulatory disturbances and hepatic oxygen deprivation in anesthesia-induced hepatotoxicity. The analysis of available data suggests that general anesthesia affects the splanchnic and hepatic circulation in various directions and to different degrees. The majority of anesthetics decreases portal blood flow in association with a decrease in cardiac output. However, hepatic arterial blood flow can be preserved, decreased, or increased. The increase in hepatic arterial blood flow, when it occurs, is usually not enough to compensate for a decrease in portal blood flow and therefore total hepatic blood flow is usually decreased during anesthesia. This decrease in total hepatic blood flow-has certain pharmacokinetic implications, namely a decrease in clearance of endogenous and exogenous substances with a high hepatic extraction ratio. On the other hand, a reduction in the hepatic oxygen supply might play a certain role in liver dysfunction occurring perioperatively. Surgical procedures–preparations combined with anesthesia have a very complex effect on the splanchnic and hepatic circulation. Within this complex, the surgical procedure–preparation plays the main role in developing circulatory disturbances, while anesthesia plays only a modifying role. Hepatic oxygen deprivation may play an important role in anesthesia-induced hepatotoxicity in different experimental models.

scholarly journals Systemic and Splanchnic Lipopolysaccharide and Endothelin-1 Plasma Levels in Liver Cirrhosis before and after Transjugular Intrahepatic Portosystemic Shunt

2016 ◽  
Vol 2016 ◽  
pp. 1-5 ◽  
Author(s):  
Jiaxiang Meng ◽  
Qing Wang ◽  
Kai Liu ◽  
Shuofei Yang ◽  
Xinxin Fan ◽  
...  
Keyword(s):  
Blood Flow ◽  
Liver Cirrhosis ◽  
Portal Hypertension ◽  
Portal Vein ◽  
Transjugular Intrahepatic Portosystemic Shunt ◽  
Bacterial Translocation ◽  
Portosystemic Shunt ◽  
Before And After ◽  
Intrahepatic Portosystemic Shunt ◽  
Cirrhotic Patients

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.

Role of glucagon in splanchnic hyperemia of chronic portal hypertension

1986 ◽  
Vol 251 (5) ◽  
pp. G674-G677 ◽  
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.

Increase in hepatic blood flow during early sepsis is due to increased portal blood flow

1991 ◽  
Vol 261 (6) ◽  
pp. R1507-R1512 ◽  
Author(s):  
P. Wang ◽  
Z. F. Ba ◽  
I. H. Chaudry
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Hepatic Blood Flow ◽  
Portal Blood Flow ◽  
Portal Blood ◽  
Arterial Blood Flow ◽  
Blood Flows ◽  
Arterial Blood ◽  
Total Hepatic Blood Flow ◽  
Early Sepsis

Although hepatic blood flow increases significantly during early sepsis [as produced by cecal ligation and puncture (CLP)], it is not known whether this is due to the increase in portal or hepatic arterial blood flows. To study this, rats were subjected to CLP, after which they and sham-operated rats received either 3 or 6 ml normal saline/100 g body wt subcutaneously (i.e., all rats received crystalloid therapy). Blood flow in various organs was determined by using a radioactive microsphere technique at 5 and 20 h after CLP or sham operation. Portal blood flow was calculated as the sum of blood flows to the spleen, pancreas, gastrointestinal tract, and mesentery. Total hepatic blood flow was the sum of portal blood flow and hepatic arterial blood flow. A significant increase in portal blood flow and in total hepatic blood flow was observed at 5 h after CLP (i.e., early sepsis), and this was not altered by doubling the volume of crystalloid resuscitation after the induction of sepsis. In contrast, hepatic arterial blood flow during early sepsis was found to be similar to control; however, it was significantly reduced in late sepsis (i.e., 20 h after CLP). Cardiac output was significantly higher than the control in early sepsis. However, even in late sepsis, cardiac output and total hepatic blood flow were not significantly different from controls. These results indicate that the increased total hepatic blood flow during early hyperdynamic sepsis is solely due to the increased portal blood flow.

scholarly journals Immediate increase in arterial blood flow in embolized hepatic segments after portal vein embolization: CT demonstration.

1998 ◽  
Vol 171 (4) ◽  
pp. 1037-1039 ◽  
Author(s):  
M Nagino ◽  
Y Nimura ◽  
J Kamiya ◽  
M Kanai ◽  
N Hayakawa ◽  
...  
Keyword(s):  
Blood Flow ◽  
Portal Vein ◽  
Portal Vein Embolization ◽  
Arterial Blood Flow ◽  
Arterial Blood

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.

Participation of adrenoceptors in liver blood flow regulation in anesthetized dogs

1987 ◽  
Vol 253 (5) ◽  
pp. H1053-H1058
Author(s):  
N. Terada ◽  
S. Koyama ◽  
J. Horiuchi ◽  
T. Takeuchi
Keyword(s):  
Blood Flow ◽  
Portal Vein ◽  
Hepatic Artery ◽  
Vascular Resistance ◽  
Adrenergic Receptors ◽  
Liver Blood Flow ◽  
Arterial Blood Flow ◽  
Tissue Blood Flow ◽  
Intact Group ◽  
Arterial Blood

We evaluated involvement of adrenergic receptors in the responses of the hepatic vasculature to reduction either of portal venous flow or hepatic arterial inflow. Portal vein occlusion caused an increase in hepatic arterial blood flow (HAF) and decreases in hepatic arterial pressure (HAP) and hepatic arterial vascular resistance (HAR) in the intact group. After pretreatment with either yohimbine or prazosin, but not propranolol, occlusion of the portal vein produced a greater decrease in HAP as compared with that in the intact group. No significant changes in HAF, HAR, or hepatic tissue blood flow (HTF) occurred after the treatment. These results indicate that the compensatory response of the hepatic arterial vasculature to altered portal blood flow (PVF) is regulated independently of the intrahepatic adrenergic receptors. Hepatic arterial occlusion caused a significant decrease in portal venous pressure, PVF, and HTF. Portal venous vascular resistance (PVR) was reduced slightly, but not significantly. After pretreatment with either yohimbine or prazosin, but not propranolol, occlusion of the hepatic artery produced an opposite effect: to increase PVF and significantly decrease PVR. These results indicate that intrahepatic alpha-adrenoceptors participate in the regulation of portal vascular tone to maintain portal vein pressure at a steady level, when inflow from the hepatic artery is reduced.

Differential effects of ATP-MgCl2 on portal and hepatic arterial blood flow after hemorrhage and resuscitation

1992 ◽  
Vol 263 (6) ◽  
pp. G895-G900 ◽  
Author(s):  
P. Wang ◽  
Z. F. Ba ◽  
I. H. Chaudry
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Hepatic Blood Flow ◽  
Portal Blood Flow ◽  
Portal Blood ◽  
Arterial Blood Flow ◽  
Shed Blood ◽  
Hepatic Arterial Blood Flow ◽  
Arterial Blood ◽  
Small Intestinal

Although ATP-MgCl2 administration after hemorrhage and resuscitation restores the decreased hepatic blood flow, it is not known whether this is due to the increase in portal blood flow or hepatic arterial blood flow. To study this, rats underwent a midline laparotomy (i.e., trauma induced) and were bled to and maintained at a mean arterial pressure of 40 mmHg until 40% of maximal shed blood volume was returned in the form of Ringer lactate (RL). The animals were resuscitated with four times the volume of the shed blood with RL, during and after which ATP-MgCl2 (50 mumol/kg body wt) or an equal volume of normal saline was infused intravenously over 95 min. Cardiac output and organ blood flow were determined by 85Sr-labeled microspheres at 90 min after the completion of resuscitation. The results indicate that portal blood flow and total hepatic blood flow decreased significantly after hemorrhage and resuscitation. ATP-MgCl2 treatment, however, restored these parameters to sham values. In contrast, hepatic arterial blood flow did not change significantly after either hemorrhage and resuscitation or ATP-MgCl2 infusion. Moreover, the depressed cardiac output was normalized and coronary blood flow was higher than shams after ATP-MgCl2 treatment. Unlike small intestinal blood flow, blood flows to the stomach, spleen, pancreas, mesentery, and cecum were not markedly affected with ATP-MgCl2 infusion. Thus the restoration of hepatic blood flow with ATP-MgCl2 treatment under such conditions is due to the increased portal blood flow, i.e., solely due to the increased small intestinal blood flow.

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