Neural activation of α-adrenoreceptors in glucose mobilization from liver

1979 ◽  
Vol 57 (9) ◽  
pp. 1037-1039 ◽  
Author(s):  
W. Wayne Lautt
Keyword(s):  
Nerve Stimulation ◽  
Adrenergic Receptors ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Venous Blood ◽  
Pressure Change ◽  
Neural Activation ◽  
Parasympathetic Nerve ◽  
Hepatic Venous Blood ◽  
Glucose Output

Using a newly described method for obtaining pure, mixed hepatic venous blood samples, it was demonstrated that glucose mobilization from the liver of the anesthetized cat in response to hepatic nerve stimulation is via α-adrenergic receptors. Neither the elevation of portal pressure nor the amount of glucose generated by the liver was affected by intraportal administration of 1 mg propranolol/kg (β blockade). In the presence of α-receptor blockade (3 mg phentolamine/kg) the portal venous pressure change was minor and the glucose output actually decreased slightly upon nerve stimulation, a response consistent with our previously demonstrated reduction of glucose output by parasympathetic nerve stimulation. The present responses to nerve stimulation were not due to activation of pancreatic nerves since these nerves were routinely ligated.

Pre- and post-sinusoidal origin of hepatic exudate in anesthetized cats

1991 ◽  
Vol 69 (12) ◽  
pp. 1914-1916 ◽  
Author(s):  
C. V. Greenway ◽  
I. R. Innes ◽  
G. D. Scott
Keyword(s):  
Steady State ◽  
Venous Pressure ◽  
Venous Blood ◽  
Portal Blood ◽  
Substantial Part ◽  
Blood Concentrations ◽  
Small Doses ◽  
Hepatic Venous Blood

In cats anesthetized with pentobarbital, hepatic venous pressure was increased to cause drops of exudate to appear on the surface of the liver. These drops were collected during steady-state infusions of small doses of ethanol and galactose when there was a large arteriovenous gradient across the liver. Comparison of the concentrations of these substances in arterial, portal, and hepatic venous blood and exudate showed that the exudate concentrations were slightly higher than the hepatic venous concentrations but markedly lower than arterial and portal blood concentrations. We conclude that the exudate cannot be entirely formed in the space of Mall (presinusoidal) but a substantial part is postsinusoidal in origin. If the exudate is a mixture of fluids equilibrated with inflowing and outflowing blood, then 75–80% of the exudate is postsinusoidal and 20–25% is presinusoidal in origin.Key words: lymph, ascites, galactose, ethanol.

Hepatic venous resistance site in the dog: localization and validation of intrahepatic pressure measurements

1987 ◽  
Vol 65 (3) ◽  
pp. 352-359 ◽  
Author(s):  
Dallas J. Legare ◽  
W. Wayne Lautt
Keyword(s):  
Blood Volume ◽  
Nerve Stimulation ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Vena Cava ◽  
Pressure Rise ◽  
Vascular Occlusion ◽  
Portal Venous Pressure ◽  
Hepatic Veins ◽  
Venous Resistance

Intrahepatic pressure (9.4 ± 0.3 mmHg; 1 mmHg = 133.32 Pa), measured proximal to a hepatic venous resistance site, was insignificantly different from portal venous pressure (9.6 ± 0.4 mmHg). This lobar venous pressure is not wedged hepatic venous pressure as it is measured from side holes in a catheter with a sealed tip. Validation of the lobar venous pressure measurement was done in a variety of ways and using different sizes and configurations of catheters. The site of hepatic venous resistance in the dog is localized to a narrow sphincterlike region about 0.5 cm in length and within 1–2 cm (usually within 1 cm) of the junction of the vena cava and hepatic veins. Sinusoidal and portal venous resistance appears insignificant in the basal state and large increases in liver blood volume (histamine infusion or passive vena caval occlusion) or large decreases in liver blood volume (passive vascular occlusion) do not alter the insignificant pressure gradient between portal and lobar venous pressures. Norepinephrine infusion (1.25 μg∙kg−1∙min−1 intraportal) and hepatic sympathetic nerve stimulation (10 Hz) led to a significantly greater rise in portal venous pressure than in lobar venous pressure, indicating some presinusoidal (and (or) sinusoidal) constriction and this indicates that lobar venous pressure cannot be assumed under all conditions to accurately reflect portal pressure. However, most of the rise in portal venous pressure induced by intraportal infusion of norepinephrine or nerve stimulation and virtually all of the pressure rise induced by histamine could be attributed to the postsinusoidal resistance site. This site was highly localized since 62% of the pressure drop from the portal vein to the inferior vena cava in the basal state occurred over a 0.5-cm length. However, the anatomical position of this site was different in the dog compared with the cat.

Effects of (±)-sotalol, (±)-propranolol, and (−)-propranolol on norepinephrine release upon hepatic nerve stimulation in the dog liver in vivo

1985 ◽  
Vol 63 (11) ◽  
pp. 1423-1428
Author(s):  
Nobuharu Yamaguchi
Keyword(s):  
Nerve Stimulation ◽  
Venous Blood ◽  
Experimental Period ◽  
Inhibitory Effect ◽  
Control Group ◽  
Beta Blocking ◽  
Hepatic Venous Blood ◽  
The Difference ◽  
Dog Liver

The study was carried out to determine whether the diminished release of norepinephrine (NE) upon sympathetic activation in the presence of sotalol can be attributed to the blockade of beta-adrenoceptors in the liver. NE release from the liver was measured in hepatic venous blood collected during direct hepatic nerve stimulation in anesthetized dogs. The mean basal NE concentration in hepatic venous and aortic blood was 0.046 ± 0.003 and 0.244 ± 0.041 ng/mL, respectively. NE release increased significantly as stimulation frequency increased, while aortic NE concentration remained unchanged. The increasing response of NE release upon stimulation in the vehicle control group remained stable during the whole experimental period. In dogs treated with sotalol (5 mg/kg, i.v.), NE release was reduced approximately by 30–43%, and the difference was statistically significant (P < 0.01) at 8 Hz. (±)-Propranolol (2.5 mg/kg, i.v.) tended to diminish it, but the difference was not significant. (−)-Propranolol (0.1 mg/kg, i.v.) did not alter NE release at any frequency tested. The beta-blocking action of these drugs in the liver, as determined by the antagonism against the hepatic arterial vasodilating response to isoproterenol, was most effective with (±)-propranolol (100%), followed by (−)-propranolol (90%) and sotalol (70%). The results suggest that the inhibitory effect of sotalol on NE release may be related to a mechanism other than its beta-blocking action in the dog liver.

Correlation between endogenous noradrenaline and glucose released from the liver upon hepatic sympathetic nerve stimulation in anesthetized dogs

1984 ◽  
Vol 62 (9) ◽  
pp. 1086-1091 ◽  
Author(s):  
Denis Garceau ◽  
Nobuharu Yamaguchi ◽  
Robert Goyer ◽  
Francine Guitard
Keyword(s):  
Nerve Stimulation ◽  
Venous Blood ◽  
Plasma Concentrations ◽  
Metabolic Role ◽  
Hepatic Venous Blood ◽  
Anesthetized Dogs ◽  
Na Release ◽  
Induced Changes ◽  
Hepatic Nerves

The metabolic role of neurally released noradrenaline (NA) was studied in the liver of anesthetized dogs. Sustained stimulation with various frequencies was directly applied on the anterior plexus of hepatic nerves. Stimulation-induced changes in plasma concentrations of endogenous catecholamines in hepatic venous blood were determined in correlation with concomitant changes in those of glucose (GL). Mean basal values for hepatic venous NA, adrenaline, dopamine, and GL were 0.062, 0.022, 0.032 ng/mL, and 97.9 mg%, respectively. Among these catecholamines, NA was the only one being released significantly during stimulation. While hepatic venous NA increased rapidly during stimulation, being maximum within 3 min, hepatic venous GL increased gradually, reaching a maximum value 5 min after the onset of stimulation. A highly significant correlation (r = 0.90, P < 0.001) was found between changes in hepatic venous NA and GL concentrations observed during stimulation at various frequencies (2–16 Hz). However, hepatic vasoconstricting responses to stimulation were not correlated with increased hepatic venous GL. An α-blockade with phentolamine (2 mg/kg, iv) resulted in diminished release of GL by approximately 50% (P < 0.05) and reduced hepatic arterial vasoconstriction by approximately 47% (P < 0.01) upon stimulation (8 Hz, 5 min), even though NA release was markedly enhanced. We conclude that in the dog, NA is the sole catecholamine released within the liver in response to direct hepatic nerve stimulation, and NA thus released mediates the hepatic glycogenolysis via α-adrenoceptors.

Galanin release during pancreatic nerve stimulation is sufficient to influence islet function

1989 ◽  
Vol 256 (1) ◽  
pp. E191-E198 ◽  
Author(s):  
B. E. Dunning ◽  
G. J. Taborsky
Keyword(s):  
Nerve Stimulation ◽  
Venous Blood ◽  
Hormone Secretion ◽  
Immunoreactive Insulin ◽  
Neural Activation ◽  
Venous Blood Flow ◽  
Concentration Difference ◽  
Specific Radioimmunoassay ◽  
Arterial Plasma ◽  
Peripheral Arterial

To determine if galanin is released during pancreatic neural activation, we measured galanin-like immunoreactivity (GLIR) in pancreatic venous and peripheral arterial plasma during 10 min of electrical stimulation of the mixed autonomic pancreatic nerves in halothane-anesthetized dogs, using a sensitive and specific radioimmunoassay. During mixed pancreatic nerve stimulation (MPNS), pancreatic venous GLIR increased by 174 +/- 20 fmol/ml, whereas arterial GLIR did not change. By use of the arteriovenous concentration difference and measurements of pancreatic venous blood flow, pancreatic spillover of GLIR was calculated and found to increase by 640 +/- 90 fmol/min during MPNS. This MPNS inhibited the output of immunoreactive insulin (IRI; delta = -53 +/- 9%) and somatostatin-like immunoreactivity (SLI, delta = -49 +/- 13%) and stimulated that of immunoreactive glucagon (IRG, delta = +600 +/- 200%). To determine if the amount of GLIR released during MPNS was sufficient to elicit these changes of pancreatic hormone secretion, we compared the effect of MPNS on IRI, SLI, and IRG output with the effect of synthetic galanin infused directly into the pancreatic artery at a rate that reproduced the MPNS-induced spillover of GLIR. Exogenous infusion of synthetic galanin (2.7 pmol/min) increased pancreatic venous levels of GLIR by 169 +/- 38 fmol/ml, did not change arterial GLIR levels, and thus increased calculated spillover (appearance) by 550 +/- 160 fmol/min, which was nearly identical to the increment produced by MPNS. This matched infusion of galanin inhibited IRI (delta = -58 +/- 3%) and SLI output (delta = -35 +/- 3%) and modestly stimulated IRG output (delta = +62 +/- 10%).(ABSTRACT TRUNCATED AT 250 WORDS)

Changes in hepatic blood volume on galactose and indocyanine green uptake by cat liver

1989 ◽  
Vol 256 (3) ◽  
pp. G524-G531 ◽  
Author(s):  
C. V. Greenway ◽  
I. R. Innes ◽  
K. L. Pushka ◽  
G. D. Scott ◽  
D. S. Sitar
Keyword(s):  
Indocyanine Green ◽  
Blood Volume ◽  
Venous Pressure ◽  
Venous Blood ◽  
Galactose Metabolism ◽  
Blood Concentrations ◽  
Hepatic Congestion ◽  
Hepatic Venous Blood ◽  
Repeated Sampling ◽  
Mild Impairment

The liver has important functions as a blood volume reserve and in uptake and metabolism of many substrates. This study examines whether changes in hepatic blood volume modify the uptakes of model substrates galactose and indocyanine green (ICG) in cats anesthetized with pentobarbital sodium. A hepatic venous long-circuit technique with an extracorporeal reservoir was used to control hepatic flow and venous pressure and to allow repeated sampling of arterial, portal, and hepatic venous blood without depletion of the cat's blood volume. Hepatic blood volume was measured by plethysmography. Galactose and ICG were infused intravenously at constant rates for 200 min in each of three series of experiments. The first series were time controls. In the second series, hepatic blood volume was increased by raising hepatic venous pressure. In the third series hepatic blood volume was decreased by hepatic nerve stimulation and infusions of norepinephrine and angiotensin. Hepatic congestion resulted in small increases in blood galactose levels, suggesting mild impairment of hepatic galactose metabolism. Decreases in liver blood volume did not modify hepatic galactose metabolism. Increases in hepatic blood volume facilitated while decreases inhibited ICG uptake, but the effects were small. Sinusoidal velocity and transit time have minor effects on uptake even for protein-bound substrates. In summary, large changes in hepatic blood volume had minor effects on galactose and ICG blood concentrations, suggesting that the metabolic functions of the liver are essentially independent of the blood reservoir function.

Autonomic nervous control of venous pressure and secretion in submandibular gland of anesthetized dogs

1998 ◽  
Vol 275 (2) ◽  
pp. G331-G341 ◽  
Author(s):  
Mary A. Lung
Keyword(s):  
Blood Flow ◽  
Submandibular Gland ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Venous Pressure ◽  
Vascular Perfusion ◽  
Sympathetic Nerve Stimulation ◽  
Nervous Control ◽  
Parasympathetic Nerve ◽  
Autonomic Nervous Control

In dogs anesthetized with pentobarbital sodium, hilar venous pressure (Phv) and secretion were measured from the submandibular gland receiving spontaneous blood flow or vascular perfusion at the normal resting flow rate. Parasympathetic nerve stimulation and ACh-induced secretion increased Phv and its pulse pressure; Phv also showed an obvious arterial (or perfusion pressure)-like waveform. Vasoactive intestinal polypeptide (VIP) exerted similar effects on Phv but produced negligible secretion. Sympathetic nerve stimulation, phenylephrine, and clonidine did not induce secretion and had no significant action on Phv, whereas isoproterenol provoked secretion and changed Phvas with parasympathetic stimulation. Background or superimposed sympathetic nerve stimulation reduced the parasympathetic nerve-induced responses; the sympathetic inhibition was abolished by phentolamine and yohimbine but not by prazosin and propranolol. The results suggest a direct relationship between Phvand secretion during parasympathetic salivation: the elevation in Phv was primarily independent of the concurrent blood flow response, mediated via muscarinic and peptidergic mechanisms, and related to an opening of arteriovenous anastomoses. Sympathetic inhibition of parasympathetic salivation may be related to prevention of an increased Phv exerted primarily via the α2-adrenergic mechanism.

Relationship between hepatic venous anatomy and hepatic venous blood loss during hepatectomy

Surgery Today ◽  
2021 ◽  
Author(s):  
Atsushi Nanashima ◽  
Yukinori Tanoue ◽  
Tatefumi Sakae ◽  
Isao Tsuneyoshi ◽  
Masahide Hiyoshi ◽  
...  
Keyword(s):  
Blood Loss ◽  
Venous Blood ◽  
Venous Anatomy ◽  
Hepatic Venous Blood ◽  
Hepatic Venous Anatomy

Off-pump direct hepatic veins-to-hemiazygos vein anastomosis after primary Kawashima operation: long-term result

2021 ◽  
pp. 1-3
Author(s):  
Renate Kaulitz ◽  
Gerhard Ziemer ◽  
Michael Hofbeck
Keyword(s):  
Venous Blood ◽  
Venous Drainage ◽  
Hepatic Veins ◽  
Off Pump ◽  
Hemiazygos Vein ◽  
Close Proximity ◽  
Hepatic Venous Blood ◽  
Balanced Distribution ◽  
Long Term Result

Abstract Direct hepatic veins-to-hemiazygos connection offers the balanced distribution of hepatic venous blood to both lungs, not requiring anticoagulation. We report a 13-year follow-up after this type of off-pump Fontan completion. Patient’s hepatic veins-to-hemiazygos confluence increased with growth to allow for unobstructed flow. This unique technique can be recommended in heterotaxy patients, if atrial hepatic venous drainage and hemiazygos vein are in close proximity.

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