Evidence for increased hepatic sympathetic nerve activity resulting in hyperglycemia in response to hemorrhage-induced reflex stimulation in anesthetized dogs

1985 ◽  
Vol 63 (9) ◽  
pp. 1209-1213 ◽  
Author(s):  
Nobuharu Yamaguchi
Keyword(s):  
Adrenal Glands ◽  
Venous Blood ◽  
Plasma Concentrations ◽  
Correlation Coefficients ◽  
Sympathetic Nerves ◽  
Maximum Output ◽  
Venous Blood Flow ◽  
Large Measure ◽  
Hepatic Venous Blood ◽  
Anesthetized Dogs

To investigate the role of the sympathoadrenal system in glucose mobilization by the liver during hemorrhage, catecholamine (CA) output from both adrenal glands was determined in anesthetized dogs. Venous blood draining from both adrenal glands was combined in a Y-tube that was connected to an electromagnetic flow probe to measure total adrenal venous blood flow. Plasma concentrations of norepinephrine (NE), epinephrine (E), dopamine (DA), and glucose (GL) were determined in various vascular regions. Adrenal CA output (nanograms per minute) under basal conditions was 50.2 ± 13.6, 181.4 ± 41.9, and 13.7 ± 4.8 for NE, E, and DA, respectively. These values were found to increase significantly (P < 0.05) in response to 5 min of hemorrhage, reaching a maximum output (nanograms per minute) of 663.6 ± 160.6 (NE), 2503.4 ± 607.8 (E), and 141.7 ± 43.7 (DA). Aortic CAs (nanograms per millilitre) increased significantly with a predominant increase in E (0.33 ± 0.08 to 3.75 ± 1.03, P < 0.05). In contrast, increases in portal and hepatic venous CAs (nanograms per millilitre) were characterized by a predominant increase in NE (0.30 ± 0.06 to 0.64 ± 0.11 and 0.17 ± 0.02 to 0.31 ± 0.07, respectively, P < 0.05). Hepatic venous and aortic GL concentrations also increased significantly during hemorrhage. Among the various correlations between plasma CA and GL concentrations, the strongest correlation was found between hepatic venous NE and hepatic venous GL (r = 0.804, P < 0.001). Correlation coefficients obtained with aortic NE and E were weaker but significant (r = 0.603 and r = 0.608, respectively, P < 0.01). Both the predominant increase in NE observed in hepatic-venous blood and the marked correlation of hepatic venous NE with hepatic venous GL suggest that, in dogs with normal sympathoadrenal systems, hemorrhage-induced hyperglycemia results from increased hepatic glycogenosis, due in large measure to increased activation of hepatic sympathetic nerves.

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.

Functional involvement of angiotensin AT2 receptor in adrenal catecholamine secretion in vivo

1999 ◽  
Vol 77 (5) ◽  
pp. 367-374 ◽  
Author(s):  
Daniel Martineau ◽  
Stéphane Lamouche ◽  
Richard Briand ◽  
Nobuharu Yamaguchi
Keyword(s):  
Adrenal Gland ◽  
High Performance ◽  
Venous Blood ◽  
Plasma Concentrations ◽  
Catecholamine Secretion ◽  
Local Administration ◽  
Venous Blood Flow ◽  
Functional Involvement ◽  
Anesthetized Dogs

The aim of the present study was to analyse modulations of adrenal catecholamine secretion from the adrenal gland of anesthetized dogs in response to locally administered angiotensin II (AngII) in the presence of either PD 123319 or CGP 42112, both of which are highly specific and selective ligands to angiotensin AT2 receptor. Plasma concentrations of epinephrine and norepinephrine in adrenal venous and aortic blood were quantified by a high performance liquid chromatography coupled with electrochemical detection (HPLC-EC) method. Adrenal venous blood flow was measured by gravimetry. Local administration of AngII (0.05 µg, 0.1 µM) to the left adrenal gland increased adrenal gland catecholamine output more than 30 times that found in nonstimulated states. Administration of either PD 123319 (0.085 µg (0.23 µM) to 8.5 µg (23 µM)) or CGP 42112 (0.005 µg (0.01 µM) to 5 µg (10 µM)) did not affect the basal catecholamine output significantly. The increase in adrenal catecholamine output in response to AngII was inhibited by ~80% following the largest dose of PD 123319. CGP 42112 significantly attenuated the catecholamine response to AngII by ~70%. PD 123319 and CGP 42112 were devoid of any agonist actions with respect to catecholamine output by the adrenal gland in vivo. Furthermore, both PD 123319 and CGP 42112 inhibited the increase in adrenal catecholamine secretion induced by local administration of AngII. The present study suggests that AT2 receptors play a role in mediating catecholamine secretion by the adrenal medulla in response to AngII receptor agonist administration in vivo.Key words: AT1 and AT2 subtypes, PD 123319, CGP 42112, AT2 antagonist, anesthetized dog.

Effects of PACAP1–27 on the canine endocrine pancreas in vivo: interaction with cholinergic mechanism

2003 ◽  
Vol 81 (7) ◽  
pp. 720-729 ◽  
Author(s):  
Nobuharu Yamaguchi ◽  
Tamar Rita Minassian ◽  
Sanae Yamaguchi
Keyword(s):  
Endocrine Pancreas ◽  
Venous Blood ◽  
Insulin Response ◽  
Glucagon Secretion ◽  
Venous Blood Flow ◽  
Dependent Manner ◽  
Cholinergic Mechanism ◽  
Insulin And Glucagon Secretion ◽  
Anesthetized Dogs

The aim of the present study was to characterize the effects of pituitary adenylate cyclase activating polypeptide (PACAP) on the endocrine pancreas in anesthetized dogs. PACAP1–27 and a PACAP receptor (PAC1) blocker, PACAP6–27, were locally administered to the pancreas. PACAP1–27 (0.005–5 μg) increased basal insulin and glucagon secretion in a dose-dependent manner. PACAP6–27 (200 μg) blocked the glucagon response to PACAP1–27 (0.5 μg) by about 80%, while the insulin response remained unchanged. With a higher dose of PACAP6–27 (500 μg), both responses to PACAP1–27 were inhibited by more than 80%. In the presence of atropine with an equivalent dose (128.2 μg) of PACAP6–27 (500 μg) on a molar basis, the insulin response to PACAP1–27 was diminished by about 20%, while the glucagon response was enhanced by about 80%. The PACAP1–27-induced increase in pancreatic venous blood flow was blocked by PACAP6–27 but not by atropine. The study suggests that the endocrine secretagogue effect of PACAP1–27 is primarily mediated by the PAC1 receptor, and that PACAP1–27 may interact with muscarinic receptor function in PACAP-induced insulin and glucagon secretion in the canine pancreas in vivo.Key words: atropine, PACAP, PAC1, muscarinic, interaction.

Effects of nifedipine and Bay K 8644 on stimulation-induced adrenal catecholamine secretion in the dog

1993 ◽  
Vol 265 (1) ◽  
pp. R28-R34 ◽  
Author(s):  
R. Gaspo ◽  
N. Yamaguchi ◽  
J. De Champlain
Keyword(s):  
Pulse Duration ◽  
Venous Blood ◽  
Plasma Concentrations ◽  
Splanchnic Nerve ◽  
Bay K 8644 ◽  
Control Group ◽  
Total Period ◽  
Aortic Blood ◽  
Anesthetized Dogs

The effects of nifedipine and BAY K 8644 on the adrenal medullary secretion in response to direct splanchnic nerve stimulation were studied in anesthetized dogs. Supramaximal stimulation (12 V) was given on the left splanchnic nerve at a frequency of 2 Hz with three different pulse durations (0.2, 2, and 20 ms) for a total period of 1.5 min. Each stimulation was given for 30 s without interruption between each stimulation. Plasma concentrations of epinephrine and norepinephrine were measured in adrenal venous and aortic blood. In the vehicle control group, epinephrine and norepinephrine concentrations in adrenal venous blood proportionally increased with the lengthening of the pulse duration without significant changes in catecholamine concentrations in aortic blood. In dogs receiving nifedipine (100 micrograms/kg iv), the net increase in adrenal venous epinephrine concentration during stimulation with 20-ms pulse duration was attenuated by approximately 50% (P < 0.05). In dogs treated with BAY K 8644 (30 micrograms.kg-1.min-1 iv), both adrenal venous epinephrine and norepinephrine secretions evoked by stimulation with 20-ms pulse duration were significantly enhanced by approximately 50%. The present results suggest that the secretion of adrenal catecholamines under in vivo conditions is controlled through mechanism(s) involving dihydropyridine sensitive L-type Ca2+ channels presumably localized on the surface of adrenal medullary chromaffin cells.

Corelease of neuropeptide Y like immunoreactivity with catecholamines from the adrenal gland during splanchnic nerve stimulation in anesthetized dogs

1990 ◽  
Vol 68 (3) ◽  
pp. 363-369 ◽  
Author(s):  
Richard Briand ◽  
Nobuharu Yamaguchi ◽  
Jacques Gagne ◽  
Tomohiko Kimura ◽  
Lisa Farley ◽  
...  
Keyword(s):  
Adrenal Gland ◽  
Neuropeptide Y ◽  
Nerve Stimulation ◽  
Plasma Concentrations ◽  
Splanchnic Nerve ◽  
Maximum Output ◽  
Burst Stimulation ◽  
High Frequencies ◽  
Anesthetized Dogs ◽  
Splanchnic Nerve Stimulation

The release of neuropeptide Y like immunoreactivity (NPY-li) from the adrenal gland was studied in relation to the secretion of catecholamines (CA:NE, norepinephrine; E, epinephrine) during the left splanchnic nerve stimulation in thiopental–chloralose anesthetized dogs (n = 16). Plasma concentrations of NE, E, and NPY-li were determined in the left adrenal venous and aortic blood. Adrenal outputs of NPY-li, NE, and E were 2.4 ± 0.4, 1.4 ± 0.2, and 7.3 ± 1.7 ng/min, under basal conditions, respectively. These values increased significantly (p < 0.05; n = 8) in response to a continuous stepwise stimulation at frequencies of 1, 3, and 10 Hz given at 3-min intervals during 9 min, reaching a maximum output of 4.6 ± 0.9 (NPY-li), 240.2 ± 50.2 (NE), and 1412.5 ± 309.7 ng/min (E) at a frequency of 10 Hz. Burst electrical stimulation at 40 Hz for 1 s at 10-s intervals for a period of 10 min produced similar increases (p < 0.05) in the release of NPY-li (4.8 ± 1.0 ng/min, n = 8), NE (283.5 ± 144.3 ng/min, n = 8), and E (1133.5 ± 430.6 ng/min, n = 8). Adrenal NPY-li output was significantly correlated with adrenal NE output (r = 0.606; n = 24; p < 0.05) and adrenal E output (r = 0.640; n = 24; p < 0.05) in dogs receiving the burst stimulation. The present findings demonstrate that NPY-li is coreleased with NE and E from the adrenal gland in response to direct splanchnic nerve stepwise or burst stimulation at high frequencies in anesthetized dogs. It is thus possible that the adrenal medullary NPY-li contributes to the modulation of circulating NPY-li levels under various physiopathological conditions.Key words: adrenal medulla, burst stimulation, catecholamines, corelease, neuropeptide Y, splanchnic nerves.

Partial extracorporeal circulation in closed-chest dogs

1959 ◽  
Vol 14 (5) ◽  
pp. 684-688 ◽  
Author(s):  
Pierre M. Galletti ◽  
Peter F. Salisbury
Keyword(s):  
Blood Flow ◽  
Venous Blood ◽  
Tissue Perfusion ◽  
Aortic Pressure ◽  
Arterial System ◽  
Venous Blood Flow ◽  
External Work ◽  
Arterial Circulation ◽  
Heart Lung Machine ◽  
Anesthetized Dogs

In anesthetized dogs a fraction of the venous blood flow was diverted into a heart-lung machine (gas exchange bag) and from there infused by gravity into the arterial circulation. During such a partial heart-lung bypass an increase in extracorporeal perfusion rate resulted in a long lasting bradycardia and a decrease of right ventricular pressure and pulmonary blood flow. The decline of the aortic pressure caused by this maneuver could be compensated by adjustment of the infusion pressure into the arterial system. The external work of the heart was reduced thereby without compromising tissue perfusion. The procedure was compatible with survival of the animals. Submitted on February 24, 1959

Pancreatic glucagon secretion during a short period of hemorrhage in anesthetized dogs

1990 ◽  
Vol 68 (7) ◽  
pp. 814-819 ◽  
Author(s):  
Richard Briand ◽  
Jacques Gagné ◽  
Nobuharu Yamaguchi
Keyword(s):  
Metabolic Response ◽  
Venous Blood ◽  
Plasma Concentrations ◽  
Glucagon Secretion ◽  
Delivery Rate ◽  
Venous Blood Flow ◽  
Pancreatic Glucagon ◽  
Hemorrhagic Hypotension ◽  
Aortic Blood ◽  
Short Period

Glucagon has been implicated in the hormonal metabolic response to hemorrhage. However, evidence for this has been obtained largely from observations of circulating plasma glucagon concentration. A clear increase in the pancreatic glucagon secretion remains to be demonstrated. Plasma concentrations of pancreatic immunoreactive glucagon (IRG) and insulin (IRI) were determined in portal venous and aortic blood, and plasma glucose in aortic blood. Dogs were bled (approximately 15 mL/kg) until aortic systolic blood pressure dropped to approximately 50% (70.5 ± 8.1 mmHg, n = 7) (1 mmHg = 133.32 Pa) of its control value (135 ± 7.1 mmHg, n = 7), and the hemorrhagic hypotension was maintained for 10 min. The net portal venous IRG delivery rate rose significantly and continued to increase during the hemorrhagic hypotension despite a significant fall in the portal venous blood flow. Aortic IRG increased significantly along with the increase in portal venous IRG delivery rate (r = 0.838, n = 42, p < 0.01). The portal venous delivery rate of IRI decreased significantly in response to hemorrhage. The aortic IRG/IRI concentration ratio increased significantly during the hemorrhage-induced hypotension. Aortic glucose concentration increased significantly 5 min after hemorrhage and continued to rise until the end of the hemorrhagic hypotension. The present study demonstrates that the secretion of pancreatic glucagon actually increases during the early phase of hemorrhage. The results also indicate that the increase in aortic IRG during the hemorrhagic hypotension is due to the increased pancreatic glucagon secretion. It is suggested that the pancreatic glucagon may be involved in the early hyperglycemic response to hemorrhage.Key words: glucagon, glucose, hemorrhage, hyperglycemia, hypotension, insulin, pancreas.

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