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.

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.

Corpuscles of Stannius and blood flow regulation in freshwater North American eels, Anguilla rostrata LeSueur

1995 ◽  
Vol 145 (1) ◽  
pp. 181-194 ◽  
Author(s):  
D G Butler ◽  
G Y Oudit
Keyword(s):  
Blood Flow ◽  
Venous Blood ◽  
Systemic Resistance ◽  
Aortic Blood Flow ◽  
Venous Blood Flow ◽  
Corpuscles Of Stannius ◽  
Blood Flows ◽  
Electrolyte Disturbances ◽  
Aortic Blood ◽  
Freshwater Eels

Abstract Cardiac output (CO), heart rate (HR), stroke volume (SV), dorsal aortic blood flow (DABF), dorsal aortic blood pressure (PDA) and plasma electrolytes were monitored in stanniectomized and sham-operated freshwater eels over a 3-week period; branchial shunting and systemic resistance (RSYS) were estimated. DABF was significantly reduced by 45% from 11·72±0·48 (control) to 6·55±0·41 (n=6; day 21) ml.min−1.kg−1 within 3 weeks after the removal of the corpuscles of Stannius. This large reduction in blood flow was due to a 25% decrease in CO and a 100% increase in estimated branchial shunting which preceded the fall in CO. CO was decreased from 16·07 ±0·31 (control) to 11·91 ±1 (n=6; day 21) ml.min−1.kg−1 through a reduction in SV; there was no significant change in HR. Estimated branchial shunting, a relative measure of branchial arterio-venous blood flow, corresponded to 2·53±0·18 ml.min−1.kg−1 (control; n=12), which represents 16% of baseline CO. Ventral and dorsal aortic pulse flows also decreased following stanniectomy. The decrease in DABF occurred in conjunction with a reduction in PDA which was measured for 12 days in a separate group of eels. Baseline PDA (3·03 ±0·1 kPa) significantly decreased by 15% to 2·55 ±0·13 kPa 4 days after stanniectomy. However, this fall in PDA was transient and accompanied by an elevation in derived RSYS. These results support the hypothesis that the corpuscles of Stannius are closely linked to cardiovascular regulation in freshwater eels. Electrolyte changes (hypercalcemia, hypomagnesia, hyperkalemia and hyponatremia) were temporally coupled to the changes in blood flows. Impaired cardiovascular function and altered patterns of blood flow to osmoregulatory organs such as the gills, kidney and skin may have led to some or all of the electrolyte disturbances which followed stanniectomy. Journal of Endocrinology (1995) 145, 181–194

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.

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.

Norethynodrel with mestranol and venous blood flow

JAMA ◽  
1966 ◽  
Vol 198 (7) ◽  
pp. 784-785 ◽  
Author(s):  
A. Neistadt
Keyword(s):  
Blood Flow ◽  
Venous Blood ◽  
Venous Blood Flow

Superior sagittal sinus thrombosis induced by thyrotoxicosis

2001 ◽  
Vol 94 (1) ◽  
pp. 130-132 ◽  
Author(s):  
Cheng-Shyuan Rau ◽  
Chun-Chung Lui ◽  
Cheng-Loong Liang ◽  
Han-Jung Chen ◽  
Yeh-Lin Kuo ◽  
...  
Keyword(s):  
Intracranial Hemorrhage ◽  
Superior Sagittal Sinus ◽  
Sinus Thrombosis ◽  
Venous Blood ◽  
Fibrinogen Concentration ◽  
Venous Blood Flow ◽  
Content Type ◽  
Sagittal Sinus ◽  
Low Protein ◽  
Diffuse Goiter

✓ There is a wide variety of disorders associated with thrombosis of the superior sagittal sinus (SSS), including infectious disease, noninfectious conditions such as vasculitis and hypercoagulable states, and complications arising from pregnancy or use of oral contraceptive medications. Despite these well-defined associations, approximately 25% of the cases remain idiopathic. In this article the authors describe a patient who was found to have SSS thrombosis while experiencing a thyrotoxic phase of Graves disease. The patient presented with intracerebral hemorrhage, subarachnoid hemorrhage, seizure, coma, a raised fibrinogen concentration, low protein C activity, and atrial fibrillations. Thrombolysis was successfully performed despite the coexistence of thrombosis and intracranial hemorrhage. Patients with thyrotoxicosis and a diffuse goiter may be predisposed to the development of SSS thrombosis, as a result of hypercoagulation and stasis of local venous blood flow. In the present case, a patient in whom thrombosis coexisted with intracranial hemorrhage was successfully treated using thrombolytic therapy.

scholarly journals Relationship between tissue factor expression and deposition of fibrin, platelets, and leukocytes on cultured endothelial cells under venous blood flow conditions

Blood ◽  
1993 ◽  
Vol 81 (8) ◽  
pp. 2050-2058 ◽  
Author(s):  
D Kirchhofer ◽  
KS Sakariassen ◽  
M Clozel ◽  
TB Tschopp ◽  
P Hadvary ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Tissue Factor ◽  
Cross Section ◽  
Leukocyte Adhesion ◽  
Venous Blood ◽  
Cell Contact ◽  
Venous Blood Flow ◽  
Necrosis Factor Alpha ◽  
Endothelial Surface ◽  
Platelet Aggregates

Abstract Endothelial cell-mediated coagulation and leukocyte adhesion are processes that might be connected by the generation of thrombin. To examine the interaction of procoagulant and proadhesive activity, cultures of endothelial cells were stimulated with tumor necrosis factor-alpha, which resulted in the surface expression of tissue factor. Subsequent exposure to human nonanticoagulated blood at a shear rate of 100 s-1 in a parallel plate perfusion device led to the deposition of polymerized fibrin, which covered 63% of the endothelial surface. In addition, numerous platelet aggregates (71 per 10 mm cross- section) and leukocytes (53 +/- 6/mm2) were deposited on stimulated endothelial cells, whereas no fibrin and only a few platelet aggregates (4 +/- 1 per 10 mm cross-section) and leukocytes (6 +/- 1/mm2) were detected on control cells. A significant portion of the adherent leukocytes bound to fibrin and platelets. However, when the deposition of fibrin and platelet aggregates was inhibited with the anti-tissue factor antibody HTFI-7B8 by 100% and 86%, respectively, leukocyte adherence remained unchanged (68 +/- 6/mm2). This indicated that leukocytes could efficiently adhere to endothelial cells through direct cell-cell contact independent of both thrombin and deposited fibrin. Moreover, this direct adhesion of leukocytes to the endothelial surface was reduced twofold to threefold when fibrin deposition occurred. These data suggest a relationship between endothelial procoagulant and proadhesive properties in that tissue factor-initiated coagulation may contribute to leukocyte adhesion through the formation of an adhesive fibrin/platelet meshwork but concurrently prevents the adhesive endothelial surface to bind leukocytes at its full capacity.

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