A New method for measurement of the ratio of hepatic arterial blood flow and portal blood flow using transumbilical portal catheterization

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

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1991.261.6.r1507 ◽

1991 ◽

Vol 261 (6) ◽

pp. R1507-R1512 ◽

Cited By ~ 4

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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Mechanism and role of intrinsic regulation of hepatic arterial blood flow: hepatic arterial buffer response

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1985.249.5.g549 ◽

1985 ◽

Vol 249 (5) ◽

pp. G549-G556 ◽

Cited By ~ 47

Author(s):

W. W. Lautt

Keyword(s):

Blood Flow ◽

Portal Blood Flow ◽

Arterial Blood Flow ◽

Portal Flow ◽

Hepatic Arterial Blood Flow ◽

Arterial Blood ◽

Total Hepatic Blood Flow ◽

Flow Changes ◽

Arterial Dilation ◽

O2 Supply

Hepatic parenchymal cell metabolic status does not control the hepatic arterial blood flow. Portal blood flow is a major intrinsic regulator of hepatic arterial tone. Hepatic arterial blood flow changes so as to buffer the impact of portal flow alterations on total hepatic blood flow, thus tending to regulate total hepatic flow at a constant level. This response is called the "hepatic arterial buffer response." The mechanism of the arterial buffer response seems to depend on portal blood flow washing away local concentrations of adenosine (production may be constant) from the area of the arterial resistance site. If portal flow decreases, less adenosine is washed away and the local concentration rises resulting in arterial dilation. Putative roles. Hepatic clearance of many hormones and endogenous compounds is blood flow limited. Constancy of total hepatic blood flow is crucial to homeostasis, and severe changes in the magnitude of flow can rapidly alter plasma concentrations of such compounds. The buffer may also prevent portal flow changes from severely altering intrahepatic blood pressures and liver blood volume. Pathological implications. If the O2 supply-to-demand ratio becomes too low, as in the case of a hypermetabolic liver (chronic alcohol exposure), a state of tissue hypoxia can exist without producing hepatic arterial dilation. Therapeutic implications. Livers show protection and improved recovery from several toxic agents, including alcohol, if the O2 supply-to-demand ratio can be increased. Arterial dilation by means of intra-arterial or intra-portal adenosine may prove useful.

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Impact of Pre Transplant Transarterial Chemoembolization on Hepatic Arterial Blood Flow and Outcomes in Liver Transplantation

10.26226/morressier.58eb975dd462b80290b50084 ◽

2017 ◽

Author(s):

Siddharth Jain

Keyword(s):

Liver Transplantation ◽

Blood Flow ◽

Transarterial Chemoembolization ◽

Arterial Blood Flow ◽

Hepatic Arterial Blood Flow ◽

Arterial Blood

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238 The effect of hepatic arterial blood flow changes on portal and hepatic venous wedged pressure in the isolated perfused CCl4-cirrhotic liver

Journal of Hepatology ◽

10.1016/s0168-8278(06)80239-4 ◽

2006 ◽

Vol 44 ◽

pp. S96 ◽

Cited By ~ 1

Author(s):

A. Zipprich ◽

M.R. Loureiro-Silva ◽

I. D'Silva ◽

R.J. Groszmann

Keyword(s):

Blood Flow ◽

Cirrhotic Liver ◽

Arterial Blood Flow ◽

Hepatic Arterial Blood Flow ◽

Arterial Blood ◽

Flow Changes

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General anesthesia and hepatic circulation

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y87-276 ◽

1987 ◽

Vol 65 (8) ◽

pp. 1762-1779 ◽

Cited By ~ 94

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.

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