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.

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.

Effect of orthotopic transplantation of liver on systemic and splanchnic hemodynamics in conscious rat

1995 ◽  
Vol 269 (1) ◽  
pp. G153-G159 ◽  
Author(s):  
L. V. Kuznetsova ◽  
D. Zhao ◽  
A. M. Wheatley
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Portal Pressure ◽  
Peripheral Resistance ◽  
Vena Cava ◽  
Cardiovascular Effects ◽  
Suture Technique ◽  
Arterial Blood Flow ◽  
Conscious Rat ◽  
Arterial Blood

The long-term cardiovascular effects of orthotopic liver transplantation (OLT) were studied in conscious Lewis rats with a radioactive microsphere technique. Three months after OLT with an all-suture technique for graft revascularization (s-OLT), all hemodynamic parameters were similar to control. OLT with "cuffs" fitted to the portal vein and infrahepatic inferior vena cava (c-OLT) led to prominent hemodynamic disturbances including 1) hyperkinetic circulation with increased cardiac index (CI; 22%; P < 0.05) and decreased mean arterial pressure (15%; P < 0.05) and total peripheral resistance (TPR; 28%; P < 0.05); 2) a slight increase in portal pressure (11.8 +/- 0.9 vs. 9.3 +/- 1.7 mmHg in control) and marked portal-systemic shunting (51 +/- 11 vs. 0.05 +/- 0.04% in control; P < 0.05); 3) increased hepatic arterial blood flow (0.49 +/- 0.06 vs. 0.27 +/- 0.04 ml.min-1.g liver wt-1; P < 0.05); 4) splanchnic vasodilation with vascular resistance significantly (P < 0.05) lower in the liver, stomach, and large intestine; and 5) increased blood flow and decreased vascular resistance in the kidneys and heart. Ganglionic blockade with chlorisondamine (5 mg/kg body wt iv) indicated that the increase in CI seen in the c-OLT rats was probably sympathetically mediated, whereas the increase in renal blood flow was a reflection of the increase in CI. After ganglionic blocker administration, TPR and regional vascular resistances decreased to approximately the same extent in the control and c-OLT groups, indicating that vascular sympathetic tone was unchanged in the c-OLT rats.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

ON THE RELATIONSHIP BETWEEN TESTICULAR BLOOD FLOW AND SECRETION OF TESTOSTERONE IN ANESTHETIZED DOGS STIMULATED WITH HUMAN CHORIONIC GONADOTROPHIN

1964 ◽  
Vol 42 (5) ◽  
pp. 671-677 ◽  
Author(s):  
Kristen B. Eik-Nes
Keyword(s):  
Blood Flow ◽  
Chorionic Gonadotrophin ◽  
Human Chorionic Gonadotrophin ◽  
Arterial Blood Flow ◽  
Constant Infusion ◽  
Left Testis ◽  
Arterial Blood ◽  
Constant Rate ◽  
Anesthetized Dogs ◽  
The Relationship

The concentration of testosterone has been measured in spermatic vein blood from the left testis in 25 anesthetized dogs, stimulated with human chorionic gonadotrophin and infused with arterial blood via the left spermatic artery at different rates. The secretion of testosterone varied with the rate at which arterial blood was infused and at a constant infusion rate of 3.81 ml/min, animals weighing from 19 to 23 kg produced testosterone at a constant rate over 90 minutes. Infusion rates lower than this decreased the secretion of testosterone, and if arterial blood was infused at a rate of 0.76 ml/min for the first 30 minutes of experimentation, the capacity of the infused testis to secrete testosterone in the ensuing 60 minutes was impaired even in animals given large doses of human chorionic gonadotrophin via the left spermatic artery. A relationship between the arterial blood flow to the testis and its ability to secrete testosterone under the influence of human chorionic gonadotrophin is thus established.

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.

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 glycerol flux after E. coli endotoxin administration

1984 ◽  
Vol 247 (4) ◽  
pp. R687-R692 ◽  
Author(s):  
O. P. McGuinness ◽  
J. J. Spitzer
Keyword(s):  
Blood Flow ◽  
Clearance Rate ◽  
Arterial Blood Flow ◽  
Metabolic Clearance ◽  
Hepatic Glucose Output ◽  
Metabolic Clearance Rate ◽  
Endotoxin Administration ◽  
Arterial Blood ◽  
Hepatic Glucose ◽  
Glucose Output

Hepatic glycerol flux was examined in dogs after the administration of Escherichia coli endotoxin (0.4 mg/kg) to determine the contribution of the liver to the previously observed decline in the metabolic clearance rate of glycerol. Hepatic glycerol flux was estimated by determining hepatic arterial and portal venous blood flows with electromagnetic flow probes and by measuring arteriovenous difference of glycerol across the liver. Administration of endotoxin significantly decreased total hepatic blood flow (by approximately 20%) but did not alter hepatic arterial blood flow. Hepatic glycerol clearance decreased by 25–30% after endotoxin administration. Hepatic glycerol extraction also decreased. Under control conditions, 60% of the metabolic clearance rate of glycerol was attributable to the liver, whereas in the postendotoxin state approximately 72% of the glycerol clearance could be accounted for by hepatic clearance. Thus changes in transhepatic glycerol flux are only partially responsible for the previously observed alterations in glycerol clearance after endotoxin administration. Although hepatic glycerol clearance decreased, net hepatic glycerol, as well as lactate and alanine, uptake did not decrease, indicating that gluconeogenic precursor availability to the hepatocytes was not diminished. Hepatic glucose output was elevated after endotoxin administration. Changes in hepatic glucose output and gluconeogenic precursor uptake help explain the endotoxin-induced alternations in the fluxes of these metabolites.

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.

H2S contributes to the hepatic arterial buffer response and mediates vasorelaxation of the hepatic artery via activation of KATP channels

2008 ◽  
Vol 295 (6) ◽  
pp. G1266-G1273 ◽  
Author(s):  
Nikolai Siebert ◽  
Daniel Cantré ◽  
Christian Eipel ◽  
Brigitte Vollmar
Keyword(s):  
Blood Flow ◽  
Portal Vein ◽  
Hepatic Artery ◽  
Buffer Capacity ◽  
Venous Blood ◽  
Control Level ◽  
Vena Cava ◽  
Arterial Blood Flow ◽  
Venous Blood Flow ◽  
Arterial Blood

Hepatic blood supply is uniquely regulated by the hepatic arterial buffer response (HABR), counteracting alterations of portal venous blood flow by flow changes of the hepatic artery. Hydrogen sulfide (H2S) has been recognized as a novel signaling molecule with vasoactive properties. However, the contribution of H2S in mediating the HABR is not yet studied. In pentobarbital-anesthetized and laparotomized rats, flow probes around the portal vein and hepatic artery allowed for assessment of the portal venous (PVBF) and hepatic arterial blood flow (HABF) under baseline conditions and stepwise reduction of PVBF for induction of HABR. Animals received either the H2S donor Na2S, DL-propargylglycine as inhibitor of the H2S synthesizing enzyme cystathionine-γ-lyase (CSE), or saline alone. Additionally, animals were treated with Na2S and the ATP-sensitive potassium channel (KATP) inhibitor glibenclamide or with glibenclamide alone. Na2S markedly increased the buffer capacity to 27.4 ± 3.0% ( P < 0.05 vs. controls: 15.5 ± 1.7%), whereas blockade of H2S formation by DL-propargylglycine significantly reduced the buffer capacity (8.5 ± 1.4%). Glibenclamide completely reversed the H2S-induced increase of buffer capacity to the control level. By means of RT-PCR, Western blot analysis, and immunohistochemistry, we observed the expression of both H2S synthesizing enzymes (CSE and cystathionine-β-synthase) in aorta, vena cava, hepatic artery, and portal vein, as well as in hepatic parenchymal tissue. Terminal branches of the hepatic afferent vessels expressed only CSE. We show for the first time that CSE-derived H2S contributes to HABR and partly mediates vasorelaxation of the hepatic artery via activation of KATP channels.

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