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.

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.

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

1985 ◽  
Vol 249 (5) ◽  
pp. G549-G556 ◽  
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.

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.

Control of hepatic arterial blood flow: independence from liver metabolic activity

1980 ◽  
Vol 239 (4) ◽  
pp. H559-H559 ◽  
Author(s):  
W. Wayne Lautt
Keyword(s):  
Blood Flow ◽  
Metabolic Activity ◽  
Hepatic Blood Flow ◽  
Venous Blood ◽  
Arterial Blood Flow ◽  
Hepatic Veins ◽  
Venous Blood Flow ◽  
Hepatic Arterial Blood Flow ◽  
Arterial Blood ◽  
Total Hepatic Blood Flow

This investigation tested the hypothesis that hepatic arterial blood flow is not dependent on hepatic metabolism, but rather is controlled in a manner that tends to maintain total hepatic blood flow constant. Cats anesthetized with pentobarbital sodium received SKF 525 A or 2,4-dinitrophenol (DNP), respectively, to inhibit or stimulate metabolism. Blood flows and oxygen uptake of the liver and gut were determined by use of a hepatic venous long circuit and noncannulating electromagnetic recording of hepatic arterial blood flow. In both sets of experiments the hepatic arterial blood flow. In both sets of experiments the hepatic artery constricted sufficiently to offset elevated portal venous blood flow, thereby maintaining total hepatic blood flow constant. The reduced hepatic arterial conductance occurred with DNP despite elevated metabolic rate and reduced oxygen in the portal and hepatic veins. Altered gut metabolism correlated with altered vascular conductance in the gut; hepatic arterial conductance changes did not correlate with changes in liver metabolic activity. The data confirmed the hypothesis. It is suggested that for hormonal homeostatis it is essential that total hepatic blood flow be regulated because hepatic clearance is flow dependent.

Splanchnic arterial blood flow in rats with portacaval shunts

1984 ◽  
Vol 246 (4) ◽  
pp. G331-G334 ◽  
Author(s):  
N. More ◽  
G. Lobosotomayor ◽  
B. Basse-Cathalinat ◽  
C. Bedin ◽  
C. Balabaud
Keyword(s):  
Blood Flow ◽  
Direct Method ◽  
Direct Consequence ◽  
Arterial Blood Flow ◽  
Liver Necrosis ◽  
Indirect Methods ◽  
Absolute Increase ◽  
Arterial Blood ◽  
Total Hepatic Blood Flow ◽  
A Direct Method

With indirect methods, it was shown in rats with portacaval shunts (PCS) that total hepatic blood flow (THBF) remained constant when expressed per gram of liver. These results implied an absolute increase in hepatic arterial blood flow (HABF). The aim of this study was to investigate HABF and splanchnic nonhepatic arterial blood flow (SNHABF) with a direct method (57Co microspheres) in PCS rats. One month after surgery, the following results were obtained in PCS rats compared with pair-fed, sham-operated rats: 1) liver mass atrophy was 42.3 +/- 10.9%, 2) HABF (ml X min-1 X g liver-1) was increased by a factor of 2.7, 3) SNHABF (ml X min-1 X 100 g body wt-1) was higher (9.8 +/- 3.3 vs. 5.6 +/- 2.7) (P less than 0.05) and 4) THBF (ml X min-1 X g liver-1) was decreased (1.36 +/- 0.34 vs. 1.85 +/- 0.86) but not significantly. Increases in HABF and SNHABF were not the direct consequence of an increase in cardiac output as attested by a normal cerebral blood flow (ml X min-1 X g organ-1) in PCS rats. In PCS rats, an increase in HABF may prevent the further spread of liver necrosis. The cause and the reason for an increase in SNHABF remain unknown.

Hepatic effect of insulin in unanesthetized normal, diabetic, and adrenalectomized dogs

1961 ◽  
Vol 201 (5) ◽  
pp. 804-810 ◽  
Author(s):  
William C. Shoemaker ◽  
Peter J. Carruthers ◽  
Ina C. Powers ◽  
Howard M. Yanof
Keyword(s):  
Blood Flow ◽  
Femoral Vein ◽  
Vena Cava ◽  
Arterial Blood Flow ◽  
Constant Infusion ◽  
Hepatic Glycogen ◽  
Arterial Blood ◽  
Total Hepatic Blood Flow ◽  
Free Glucose ◽  
Glucose Output

Measurement of arterial, portal, and hepatic venous plasma glucose concentrations were made in unanesthetized dogs whose hepatic vessels were previously catheterized. Total hepatic blood flow was measured by a modified Bromsulphalein method and hepatic arterial blood flow by a trapezoidal wave electromagnetic blood flowmeter. Serial biopsies of the liver were obtained, also under unanesthetized conditions, for measurement of glycogen and free glucose. Various doses of glucagon-free insulin were given by a single, rapid, intravenous injection or by a constant infusion directly into the liver via portal vein and via femoral vein or vena cava. Insulin was administered in normal, in adrenalectomized, in depancreatized, and in depancreatized-adrenalectomized dogs. Under each of the conditions observed insulin produced no decrease in the hepatic glucose output. Moreover, no increased hepatic glycogen or free glucose concentrations were found in hepatic biopsies after insulin administration.

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.

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