Hepatic parasympathetic neural effect on glucose balance in the intact liver

Sympathetic nerves to the intact liver of the cat were selectively destroyed by injection of 6-hydroxydopamine into the portal vein 1 week prior to the experiment. Glucose output was calculated from the product of the arterial–venous glucose difference and hepatic blood flow. Hepatic blood flow was monitored by an electromagnetic flowmeter using a hepatic venous long-circuit. Stimulation of the parasympathetic nerves isolated from around the common hepatic artery produced a rapid reduction in hepatic glucose output to one-quarter of control levels by 2 min and to zero by 10 min of nerve stimulation. The data show that hepatic glucose balance is readily influenced by the hepatic parasympathetic nerves.

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Hepatic glucose balance in response to direct stimulation of sympathetic nerves in the intact liver of cats

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y78-163 ◽

1978 ◽

Vol 56 (6) ◽

pp. 1022-1028 ◽

Cited By ~ 26

Author(s):

W. Wayne Lautt ◽

Chong Wong

Keyword(s):

Sympathetic Nerves ◽

Direct Stimulation ◽

Blood Flows ◽

Parasympathetic Nerves ◽

Hepatic Glucose ◽

Simultaneous Activation ◽

Glucose Output ◽

Hepatic Nerves ◽

Mixed Nerve ◽

Stimulation Of

Changes in hepatic glucose balance in response to direct stimulation of the hepatic nerves were measured in cats. Simultaneous measurements were made of glucose concentrations entering and leaving the intact liver; this, combined with measured blood flows, allows calculation of hepatic glucose balance. Stimulation of the hepatic sympathetic nerves (8 Hz, 15 V, 1 ms) produced a rapid increase in hepatic glucose output that was statistically significant after 1 min and reached a peak 3–5 min after onset of stimulation, after which time the output declined somewhat. The half time for deactivation of the response was 1.8–2 min. Variability in the responses was largely accounted for by the variable control base lines measured immediately prior to stimulation. Those animals showing the highest basal output showed the least increase in output in response to the nerves. The response to stimulation of the mixed nerve trunk in the presence and absence of atropine (1 mg/kg, intraportal) was similar. Simultaneous activation of hepatic sympathetic and parasympathetic nerves therefore produces a purely sympathetic type of effect on net glucose balance across the liver. It was also shown that changes in net splanchnic output or simply in arterial – hepatic venous glucose differences are an adequate reflection of liver glucose balance under the currently tested responses.

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Measurement of hepatic glucose output and hepatic blood flow in response to glucagon

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1959.196.2.315 ◽

1959 ◽

Vol 196 (2) ◽

pp. 315-318 ◽

Cited By ~ 44

Author(s):

William C. Shoemaker ◽

Theodore B. Van Itallie ◽

William F. Walker

Keyword(s):

Blood Flow ◽

Hepatic Blood Flow ◽

Glucose Concentration ◽

Base Line ◽

Hepatic Glucose Output ◽

Marked Rise ◽

Hepatic Glucose ◽

The Mean ◽

Glucose Output ◽

Venous Glucose

Arterial, portal and hepatic venous glucose concentrations and hepatic blood flow were simultaneously measured in nine dogs in the postabsorptive state, and after intravenous administration of glucagon. A marked rise in hepatic venous glucose concentration occurred promptly after glucagon administration. This rise coincided with a mean increase in estimated hepatic blood flow of approximately 100%. This increase in hepatic blood flow following the administration of glucagon was regularly observed in all animals; the increase in blood flow ranged from 41 to 204% in this series. Hepatic glucose output was calculated by multiplying the portal-hepatic vein gradient by the hepatic blood flow. The mean hepatic glucose output of the series increased from base line of 73 mg/min. to a maximum of 381 mg/min. in response to glucagon.

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Estimation of the hepatic blood flow in the dog with the Xe133 and hydrogen wash-out, Au198-colloid uptake techniques and with the electromagnetic flowmeter

Research in Experimental Medicine ◽

10.1007/bf01851340 ◽

1976 ◽

Vol 169 (1) ◽

pp. 69-76 ◽

Cited By ~ 9

Author(s):

G. Szabó ◽

I. Benyó ◽

J. Sándor ◽

Z. Benyó

Keyword(s):

Blood Flow ◽

Hepatic Blood Flow ◽

Electromagnetic Flowmeter

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Hepatic lactate uptake versus leg lactate output during exercise in humans

Journal of Applied Physiology ◽

10.1152/japplphysiol.00027.2007 ◽

2007 ◽

Vol 103 (4) ◽

pp. 1227-1233 ◽

Cited By ~ 23

Author(s):

H. B. Nielsen ◽

M. A. Febbraio ◽

P. Ott ◽

P. Krustrup ◽

N. H. Secher

Keyword(s):

Blood Flow ◽

Glucose Uptake ◽

Prolonged Exercise ◽

Incremental Exercise ◽

Hepatic Glucose Output ◽

Arterial Lactate ◽

Hepatic Glucose ◽

Lactate Output ◽

Lactate Uptake ◽

Glucose Output

The exponential rise in blood lactate with exercise intensity may be influenced by hepatic lactate uptake. We compared muscle-derived lactate to the hepatic elimination during 2 h prolonged cycling (62 ± 4% of maximal O2 uptake, V̇o2max) followed by incremental exercise in seven healthy men. Hepatic blood flow was assessed by indocyanine green dye elimination and leg blood flow by thermodilution. During prolonged exercise, the hepatic glucose output was lower than the leg glucose uptake (3.8 ± 0.5 vs. 6.5 ± 0.6 mmol/min; mean ± SE) and at an arterial lactate of 2.0 ± 0.2 mM, the leg lactate output of 3.0 ± 1.8 mmol/min was about fourfold higher than the hepatic lactate uptake (0.7 ± 0.3 mmol/min). During incremental exercise, the hepatic glucose output was about one-third of the leg glucose uptake (2.0 ± 0.4 vs. 6.2 ± 1.3 mmol/min) and the arterial lactate reached 6.0 ± 1.1 mM because the leg lactate output of 8.9 ± 2.7 mmol/min was markedly higher than the lactate taken up by the liver (1.1 ± 0.6 mmol/min). Compared with prolonged exercise, the hepatic lactate uptake increased during incremental exercise, but the relative hepatic lactate uptake decreased to about one-tenth of the lactate released by the legs. This drop in relative hepatic lactate extraction may contribute to the increase in arterial lactate during intense exercise.

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Hemodynamic Effects of CCl4 in the Intact Liver of the Cat

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y74-093 ◽

1974 ◽

Vol 52 (3) ◽

pp. 727-735 ◽

Cited By ~ 8

Author(s):

W. W. Lautt ◽

G. L. Plaa

Keyword(s):

Blood Flow ◽

Hepatic Blood Flow ◽

Sympathetic Nerves ◽

Causative Factor ◽

Arterial Infusion ◽

Total Blood ◽

Arterial Blood ◽

Reflex Activation ◽

Total Blood Flow ◽

Early Phases

Blood flow in the intact liver of anesthetized cats did not change significantly over a period of 4 h following intraduodenal injection of CCl4 (1 ml/kg). Hepatocellular disruption was well underway by 2 h after the injection. Twenty-four hours following an oral dose of CCl4, the hepatic arterial resistance to blood flow was reduced and total blood flow to the liver was at least as high as in control animals. At this time, the hepatic artery appeared fully dilated and was less responsive to humoral (intra-arterial infusion of noradrenaline) and neural (reflex activation of the sympathetic nerves) constrictor influences. Thus, alterations in hepatic blood flow do not occur during the early phases of CCl4-induced hepatic injury. These data indicate that diminished blood flow is not a causative factor in the initial phases of CCl4-induced liver injury. By 24 h, hepatic blood flow is altered in such a manner that the damaged liver receives a higher proportion of arterial blood and a total blood flow that is not reduced in spite of a generally depressed cardiovascular system.

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Mechanism of action of vasoconstrictor responses to atriopeptin II in conscious SHR

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1985.249.6.r781 ◽

1985 ◽

Vol 249 (6) ◽

pp. R781-R786 ◽

Cited By ~ 1

Author(s):

R. W. Lappe ◽

J. A. Todt ◽

R. L. Wendt

Keyword(s):

Blood Flow ◽

Arterial Pressure ◽

Vascular Resistance ◽

Regional Blood Flow ◽

Sympathetic Nerves ◽

Spontaneously Hypertensive ◽

Regional Vascular Resistance ◽

6 Hydroxydopamine ◽

Renal Vascular ◽

Renal Sympathetic

Previous studies have demonstrated that infusion of synthetic atriopeptin II (AP II) lowered arterial pressure, reduced regional blood flow, and increased total peripheral and regional vascular resistances in conscious spontaneously hypertensive rats (SHR). This study was designed to examine the mechanism(s) involved in regional vasoconstrictor responses to AP II. In these experiments, hemodynamic actions of AP II were examined in control, 6-hydroxydopamine-treated (chemically sympathectomized), and renal-denervated groups of instrumented conscious SHR. Infusion of AP II (1 microgram X kg-1 X min-1) caused similar reductions in mean arterial pressure in control (-22 +/- 2 mmHg), chemically sympathectomized (-23 +/- 2 mmHg), and renal-denervated (-23 +/- 3 mmHg) SHR. In control SHR, AP II infusion reduced renal (-20 +/- 3%), mesenteric (-26 +/- 2%), and hindquarters (-18 +/- 10%) blood flow and increased regional vascular resistance in all three beds. Chemical sympathectomy prevented the fall in renal blood flow (RBF) and significantly abolished the regional vasoconstrictor responses to AP II infusion. In unilateral renal-denervated groups of SHR, AP II reduced renal vascular resistance (RVR) -11 +/- 3% but failed to alter RBF (-3 +/- 1%) in denervated kidneys. In contrast, RVR increased (20 +/- 7%) and RBF was significantly reduced (-29 +/- 3%) in contralateral-innervated kidneys. This study demonstrated that chemical or surgical destruction of renal sympathetic nerves abolished AP II-induced increases in RVR. These data further indicate that in conscious SHR the regional vasoconstrictor responses to AP II infusion appear to be mediated by increases in sympathetic tone rather than through direct vascular actions of AP II.

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HEPATIC BLOOD FLOW AND GLUCOSE OUTPUT IN NORMAL UNANESTHETIZED DOGS

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1947.148.2.302 ◽

1947 ◽

Vol 148 (2) ◽

pp. 302-311 ◽

Cited By ~ 17

Author(s):

Alys Lipscomb ◽

Lathan A. Crandall

Keyword(s):

Blood Flow ◽

Hepatic Blood Flow ◽

Glucose Output

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Blood flow and nutrient exchange across the liver and gut of the dairy cow

British Journal Of Nutrition ◽

10.1079/bjn19830057 ◽

1983 ◽

Vol 49 (3) ◽

pp. 481-496 ◽

Cited By ~ 122

Author(s):

M. A. Lomax ◽

G. D. Baird

Keyword(s):

Fatty Acids ◽

Blood Flow ◽

Flow Rate ◽

Ketone Bodies ◽

Blood Flow Rate ◽

Hepatic Uptake ◽

Hepatic Glucose Output ◽

Lactating Cows ◽

Hepatic Glucose ◽

Glucose Output

1. The rate of blood flow in the portal and hepatic veins, and the net exchange across the gut and liver of volatile fatty acids (VFA), glucose, lactate, pyruvate, amino acids, ketone bodies, glycerol, non-esterified fatty acids (NEFA) and oxygen, were measured in lactating and non-lactating cows (a) in the normal, fed state and (b) before, during and after 6 d of fasting.2. Blood flow rate through the liver was 52% higher in normal, fed, lactating cows as compared with non-lactating cows, and was decreased by fasting in both groups of cows. Portal blood flow rate increased with an increase in metabolizable energy (ME) intake.3. Lactating, as compared with non-lactating, cows exhibited lower arterial concentrations of glucose and lactate, higher net portal outputs of VFA and ketone bodies, a higher net hepatic output of glucose, and higher net hepatic uptakes of propionate and lactate. The splanchnic outputs of acetate, glucose and hydroxybutyrate were all apparently greater in the lactating cows.4. Fasting caused a rapid decrease in the blood concentrations of the VFA and an increase in those of glycerol and NEFA. The portal, i.e. gut, outputs of VFA, lactate, ketone bodies, alanine and (serine+threonine), and the portal uptake of O2, were all decreased by fasting. Fasting for 6 h also decreased the hepatic output of glucose and acetate by 77 and 95% respectively, increased the hepatic uptake of pyruvate, glycerol and NEFA, and doubled hepatic ketone-body output. The splanchnic output of acetate and glucose and the splanchnic uptake of O2 were also decreased by fasting.5. The net portal outputs of VFA, lactate and hydroxybutyrate, and the net hepatic output of glucose, were all correlated with ME intake in fed and fasted cows. Hepatic glucose output was also correlated with milk yield.6. The net hepatic uptake of gluconeogenic precursors measured in this study could account for net hepatic glucose output in the fasted cows, but not in the fed cows. The net hepatic uptake of the ketogenic precursors butyrate and NEFA was sufficient to account for the hepatic output of ketone bodies in both fed and fasted cows, but it is unlikely that the hepatic uptake of ketogenic precursors could also account for the observed hepatic output of acetate.

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