Plasma Glucagon in Experimental Posthemorrhagic Shock

Halmagyi, D; Neering, I. R.; Lazarus, L.; Jd, Young; Pullin, Joy

doi:10.1097/00005373-196904000-00004

Cited by 24 publications

(14 citation statements)

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“…Hypovolemia-induced hyperglucagonemia has been studied largely as a consequence of its relevance to trauma and shock [12,15,18] and the consensus from experiments conducted in sheep, dogs and cats is that while the magni tude of the response can be reduced by surgical or phar macological interventions, it is not completely eliminated by autonomic blockade [12,18] or by sectioning of the splanchnic nerve alone or in combination with adrenalec tomy [2]. In addition, hypotensive hyperglucagonemia in duced by isolation of the carotid baroreceptors in vagotomized cats is depressed, but by no means eliminated, by adrenalectomy, splanchnicectomy or pancreatic sympa thectomy [14].…”

Section: Discussionmentioning

confidence: 99%

“…Realizing that such levels are of the order of those attained in the circulation during hypovolemia and other traumatic stresses [16, 17] and that such situations are also characterized by increases in circulating levels of glu cagon [12,15], we undertook an investigation of the hypo thesis that the increased secretory activity of the pancreatic a-cells might at least in part be attributable to the influ ence of the high circulating levels of OT and AVP. We have therefore examined the influence of passive immunization against AVP and OT on the appearance of glucagon in the circulation of rats subjected to hemorrhage.…”

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confidence: 99%

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Evidence for Participation of the Neurohypophysial Hormones in the Hyperglucagonemic Response to Hemorrhage in the Rat

Be¹,

Jg²,

Cp³

1985

Neuroendocrinology

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Conscious adult male rats bearing jugular cannulae were injected with either normal rabbit serum (NRS) or with serum containing antibodies to both oxytocin (OT) and arginine vasopressin (AVP). In the NRS-treated group, plasma levels of OT, AVP and immunoreactive glucagon (IRG) were significantly elevated 10 min after hemorrhage (2.3 ml/100 g body weight over 5 min) whereas hyperglucagonemia was not detected in the antiserum-treated group until 30 min posthemorrhage. In animals which were deprived of water during the experiment, plasma IRG in the antiserum-treated group reached only 40% of the levels in the NRS-treated controls. These results suggest that hemorrhage-induced elevations in circulating AVP and/or OT contribute to increased release of glucagon by the endocrine pancreas consistent with previous demonstration of glucagonotropic activity of synthetic neurohypophysial peptides.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Evidence for Participation of the Neurohypophysial Hormones in the Hyperglucagonemic Response to Hemorrhage in the Rat

Be¹,

Jg²,

Cp³

1985

Neuroendocrinology

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“…The present data suggest that these nerves contribute to the normal adjustment of insulin secretion during haemorrhagic hypotension and it seems likely that they are involved in the inhibition of insulin release during other stress situations as well. Today, pancreatic glucagon is considered as one of the 'stress hormones' since its plasma concentration is markedly increased during different types of stress such as haemorrhage and haemorrhagic shock (11,16,21,29), burns (33), trauma (20,22,24), and myocardial infarction (32). The mechanism(s) by which glucagon is released in these situations are not clear but a role for the sympatho-adrenal system has been postulated, since catecholamines promote glucagon release in vivo and in vitro (31).…”

Section: Discussionmentioning

confidence: 99%

Role of the Sympatho-Adrenal System in the Control of Endocrine Pancreas during Haemorrhage in Cats

Andersson¹,

Hoist²,

Järhult³

1979

Eur Surg Res

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Glucose, insulin and glucagon concentrations were determined before, during and after a 60-min period of haemorrhagic hypotension at 60 mm Hg in controls, adrenal-ectomized and splanchnicectomized cats. Peak increase of arterial plasma glucose concentration in response to haemorrhage was 13.7 ± 4.3 mM in controls, 10.2 ± 2.8 mΛf in adrenal-ectomized and 3.1 ± 1.7 mM in splanchnicectomized cats, respectively. Peak portal insulin decrease was 58 ± 8 and 36 ± 14 pmol/l in controls and adrenalectomized cats, respectively, whereas insulin levels increased slightly in splanchnicectomized cats during hypovolaemia. Portal plasma glucagon concentration rose by about 250 pmol/l in response to bleeding in all groups of cats. We conclude that the prompt hyperglycaemic and hypomsuünaemic response to haemorrhage in cats are caused by an adrenergic, ‘non-medullary’ mechanism, whereas the marked rise in pancreatic glucagon release seems due to factors unrelated to the sympatho-adrenal system.

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“…Elevated levels of glucagon in experimental hemorrhagiC shock are of unknown significance. 47 Release of catecholamines from the adrenal has provided the basis for a provocative test for pheochromocytomaYo Glucagon augmented renal electrolyte clearance in the dog/ 2 , 97, 114 which was associated with an unsustained rise in glomerular filtration rate and renal plasma flow. l09 No striking changes in clearance of insulin, creatinine, sodium, potassium, and chloride (nor serum changes in the later three) were demonstrable in man.…”

Section: Extracardiac and Metabolic Effectsmentioning

confidence: 99%

Glucagon: Present status in cardiovascular disease

Kones

Phillips

1971

Clin Pharma and Therapeutics

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The actions of pancreatic glucagon, a known hyperglycemic, hypoaminoacidemic, and lipolytic agent, have received recent attention because of a variety of effects mediated by increases in cyclic AMP concentrations. Studies in the dog demonstrated the positive inotropic and chronotropic actions of glucagon, unaltered by reserpine, insulin, or propranolol. Enhanced contractility was additive with that of the digitalis preparations but did not produce undesirable arrhythmias. The ability of glucagon to increase contractility was attenuated with longer duration of experimental congestive heart failure, thus implying greater effectiveness in acute pathology. In man, variables dependent upon contractility are correspondingly enhanced with the use of glucagon. Current evidence suggests glucagon is a secondary coronary vasodilator and lowers renal vascular resistance as well. improvement have been noted as a result of continuous glucagon therapy in patients with early congestive heart failure, cardiogenic shock, myocardial infarction, and in low output syndromes following open heart surgery. Glucagon appears to activate adenyl cyclase to increase cycliC AMP levels, which in tum enlarges the intracellular calcium pool. Thus, according to current excitation-contraction theories, an increase in contractility results.Extracardiac and metabolic effects

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Plasma Glucagon in Experimental Posthemorrhagic Shock

Cited by 24 publications

References 0 publications

Evidence for Participation of the Neurohypophysial Hormones in the Hyperglucagonemic Response to Hemorrhage in the Rat

Evidence for Participation of the Neurohypophysial Hormones in the Hyperglucagonemic Response to Hemorrhage in the Rat

Role of the Sympatho-Adrenal System in the Control of Endocrine Pancreas during Haemorrhage in Cats

Glucagon: Present status in cardiovascular disease

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