Is it feasible to monitor total hepatic blood flow by use of transesophageal echography? An experimental study in pigs

2001 ◽  
Vol 27 (3) ◽  
pp. 580-585 ◽  
Author(s):  
Wolfram Schütz ◽  
Rainer Meierhenrich ◽  
Karl Träger ◽  
Albrecht Gauss ◽  
Peter Radermacher ◽  
...  
Keyword(s):  
Experimental Study ◽  
Blood Flow ◽  
Hepatic Blood Flow ◽  
Total Hepatic Blood Flow

scholarly journals Changes in Hepatic Hemodynamics due to Primary Liver Tumours

HPB Surgery ◽  
1996 ◽  
Vol 9 (4) ◽  
pp. 245-248 ◽  
Author(s):  
F. Jakab ◽  
Z. Ráth ◽  
F. Schmal ◽  
P. Nagy ◽  
J. Faller
Keyword(s):  
Hepatocellular Carcinoma ◽  
Blood Flow ◽  
Hepatic Artery ◽  
Hepatic Blood Flow ◽  
Primary Hepatocellular Carcinoma ◽  
Portal Venous Flow ◽  
Venous Flow ◽  
Control Value ◽  
Early Results ◽  
Total Hepatic Blood Flow

Data regarding the afferent circulation of the liver in patients with primary hepatocellular carcinoma are controversial, we have carried out measurement of hepatic arterial and portal venous flow intraoperatively by transit time ultrasonic volume flowmetry. In patients with primary hepatocellular carcinoma the hepatic artery flow increased to 0.55±0.211 compared with the control value of 0.37±0.102 1/min. (p<0.01). The portal venous flow decreased from 0.61±0.212 l/min, to 0.47±l/min. p<0.01). Due to the opposite changes in the afferent circulation the total hepatic blood flow did not change significantly, compared with controls.The ratio of hepatic arterial flow to portal vein flow increased to 1.239±0.246 in patients with hepatocellular carcinoma, which is double of the control value (0.66±0.259 l/min). After resection this ratio did not change.The resection did not alter hepatic artery or portal venous flow significantly, although the total hepatic blood flow decreased significantly (p<0.01).On the basis of our early results it is possible that the ratio of the two circulations may be to deel measured with doppler ultrasound and provide diagnostic information.

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.

Hepatic venular resistance responses to norepinephrine, isoproterenol, adenosine, histamine, and ACh in rabbits

1998 ◽  
Vol 274 (3) ◽  
pp. H777-H785 ◽  
Author(s):  
Carl F. Rothe ◽  
Roberto Maass-Moreno
Keyword(s):  
Blood Flow ◽  
Portal Vein ◽  
Hepatic Blood Flow ◽  
Inferior Vena ◽  
Liver Volume ◽  
Liver Lobe ◽  
Inferior Vena Caval ◽  
Total Hepatic Blood Flow ◽  
Constant Rate ◽  
Increased Blood Flow

Changes in hepatic venous resistance were estimated in rabbits from the hepatic venular-inferior vena caval pressure gradient [servo-null micropipettes in 49 ± 15 (SD) μm vessels] and the total hepatic blood flow (ultrasound probe encircling the hepatic artery and the portal vein). Changes in liver volume, and thus vascular capacitance, were estimated from measures of the liver lobe thickness. Norepinephrine (NE), isoproterenol (Iso), adenosine (Ado), histamine (Hist), or acetylcholine (ACh) was infused into the portal vein at a constant rate for 5 min. NE, Hist, and Ado increased hepatic venular pressure, but only NE and Hist significantly increased hepatic venular resistance. NE reduced the liver thickness, but Hist and Ado caused engorgement. Hepatic blood flow was increased by NE and Ado and decreased by ACh. The influence of intraportal vein infusion of Iso on the liver vasculature, at doses similar to that of NE, was insignificant. We conclude that NE acted on all the hepatic microvasculature, increasing resistance and actively decreasing vascular volume. Hist passively induced engorgement by increasing outflow resistance, whereas the liver engorgement seen with Ado was passively related to the increased blood flow. ACh constricted the portal venules but did not change the liver volume.

Experimental study of the effect of intraportal prostaglandin E1 on hepatic blood flow during reperfusion after ischaemia and hepatectomy

1999 ◽  
Vol 86 (6) ◽  
pp. 776-783 ◽  
Author(s):  
M. A. Hossain ◽  
I. Hamamoto ◽  
H. Wakabayashi ◽  
F. Goda ◽  
S. Kobayashi ◽  
...  
Keyword(s):  
Experimental Study ◽  
Blood Flow ◽  
Hepatic Blood Flow ◽  
Prostaglandin E1

Evidence for the association between total hepatic blood flow and hepatic glutathione content

1986 ◽  
Vol 35 (10) ◽  
pp. 1629-1632 ◽  
Author(s):  
Walter G. Bottje ◽  
Aslam S. Hassan ◽  
Kenneth R. Holmes
Keyword(s):  
Blood Flow ◽  
Hepatic Blood Flow ◽  
Total Hepatic Blood Flow ◽  
Hepatic Glutathione

scholarly journals Effect of histamine H2-receptor antagonists on the total hepatic blood flow in patients with chronic liver diseases.

Kanzo ◽  
1986 ◽  
Vol 27 (7) ◽  
pp. 908-914 ◽  
Author(s):  
Kouichi AKAMATSU ◽  
Souichiro MIYAUCHI ◽  
Kenya MURASE ◽  
Yuji WATANABE ◽  
Nobuo NISHIMURA ◽  
...  
Keyword(s):  
Blood Flow ◽  
Hepatic Blood Flow ◽  
Liver Diseases ◽  
Chronic Liver ◽  
Chronic Liver Diseases ◽  
Receptor Antagonists ◽  
H2 Receptor Antagonists ◽  
Histamine H2 Receptor ◽  
H2 Receptor ◽  
Total Hepatic Blood Flow

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.

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