Splanchnic neural regulation of somatostatin secretion in the isolated perfused human pancreas

F. C. Brunicardi, D. Elahi, Dana Andersen

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Objective: The somatostatin-secreting delta cells in the islets of Langerhans appear to be regulated by neural mechanisms that have not been defined clearly. In this study, the celiac neural bundle of the human pancreas was electrically stimulated in the presence and absence of selective neural antagonists. Summary Background Data: The authors previously reported on studies of the splanchnic neural regulation of insulin, glucagon, and pancreatic polypeptide secretion. In these studies, alpha-adrenergic fibers appeared to have a predominant effect, strongly inhibiting the secretion of insulin, glucagon, and pancreatic polypeptide secretion. Cholinergic fibers appeared to stimulate strongly, although beta-adrenergic fibers weakly stimulated, the secretion of these hormones. Investigations of neural regulatory mechanisms governing human somatostatin release in vitro have not been previously reported. Methods: Pancreata were obtained from eight cadaveric organ donors. The isolated perfused human pancreas technique was used to assess the regulation of somatostatin secretion by the various neural fibers contained within the celiac plexus. The secretory response of somatostatin was examined in the presence of 16.7 mmol/L glucose, with and without neural stimulation, and specific neural antagonists. Results: The basal somatostatin secretion was 88 ± 26 fmol/g/min and increased 131 ± 23% (n = 8, p <0.01) in response to 16.7 mmol/L glucose. The augmentation seen with glucose was inhibited 66 ± 22% (n = 8, p <0.05) during celiac neural bundle stimulation. Alpha-adrenergic blockade resulted in a 90 ± 30% (n = 6, p <0.01) augmentation of somatostatin release. Beta-adrenergic blockade caused a 13 ± 2% (n = 6, p <0.05) suppression of somatostatin release. Complete adrenergic blockade resulted in a 25 ± 23% (n = 5, p = not significant) inhibition of somatostatin release. Cholinergic blockade resulted in a 40 ± 10% (n = 6, p <0.02) suppression of somatostatin release. Conclusions: The predominant effect of celiac neural bundle stimulation was inhibition of somatostatin secretion through an alpha- adrenergic effect. Beta-adrenergic fibers stimulate somatostatin secretion; cholinergic fibers have a negligible effect on somatostatin secretion. These data suggest that the splanchnic innervation of the pancreas has a potent regulatory role in somatostatin release in this in vitro human model.

Original languageEnglish (US)
Pages (from-to)258-266
Number of pages9
JournalAnnals of Surgery
Volume219
Issue number3
StatePublished - 1994
Externally publishedYes

Fingerprint

Viscera
Somatostatin
Pancreas
Adrenergic Fibers
Adrenergic Agents
Cholinergic Fibers
Abdomen
Pancreatic Polypeptide
Somatostatin-Secreting Cells
Glucagon
Glucose
Celiac Plexus
Insulin
Islets of Langerhans
Cholinergic Agents
Tissue Donors
Hormones

ASJC Scopus subject areas

  • Surgery

Cite this

Splanchnic neural regulation of somatostatin secretion in the isolated perfused human pancreas. / Brunicardi, F. C.; Elahi, D.; Andersen, Dana.

In: Annals of Surgery, Vol. 219, No. 3, 1994, p. 258-266.

Research output: Contribution to journalArticle

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title = "Splanchnic neural regulation of somatostatin secretion in the isolated perfused human pancreas",
abstract = "Objective: The somatostatin-secreting delta cells in the islets of Langerhans appear to be regulated by neural mechanisms that have not been defined clearly. In this study, the celiac neural bundle of the human pancreas was electrically stimulated in the presence and absence of selective neural antagonists. Summary Background Data: The authors previously reported on studies of the splanchnic neural regulation of insulin, glucagon, and pancreatic polypeptide secretion. In these studies, alpha-adrenergic fibers appeared to have a predominant effect, strongly inhibiting the secretion of insulin, glucagon, and pancreatic polypeptide secretion. Cholinergic fibers appeared to stimulate strongly, although beta-adrenergic fibers weakly stimulated, the secretion of these hormones. Investigations of neural regulatory mechanisms governing human somatostatin release in vitro have not been previously reported. Methods: Pancreata were obtained from eight cadaveric organ donors. The isolated perfused human pancreas technique was used to assess the regulation of somatostatin secretion by the various neural fibers contained within the celiac plexus. The secretory response of somatostatin was examined in the presence of 16.7 mmol/L glucose, with and without neural stimulation, and specific neural antagonists. Results: The basal somatostatin secretion was 88 ± 26 fmol/g/min and increased 131 ± 23{\%} (n = 8, p <0.01) in response to 16.7 mmol/L glucose. The augmentation seen with glucose was inhibited 66 ± 22{\%} (n = 8, p <0.05) during celiac neural bundle stimulation. Alpha-adrenergic blockade resulted in a 90 ± 30{\%} (n = 6, p <0.01) augmentation of somatostatin release. Beta-adrenergic blockade caused a 13 ± 2{\%} (n = 6, p <0.05) suppression of somatostatin release. Complete adrenergic blockade resulted in a 25 ± 23{\%} (n = 5, p = not significant) inhibition of somatostatin release. Cholinergic blockade resulted in a 40 ± 10{\%} (n = 6, p <0.02) suppression of somatostatin release. Conclusions: The predominant effect of celiac neural bundle stimulation was inhibition of somatostatin secretion through an alpha- adrenergic effect. Beta-adrenergic fibers stimulate somatostatin secretion; cholinergic fibers have a negligible effect on somatostatin secretion. These data suggest that the splanchnic innervation of the pancreas has a potent regulatory role in somatostatin release in this in vitro human model.",
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AU - Brunicardi, F. C.

AU - Elahi, D.

AU - Andersen, Dana

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Y1 - 1994

N2 - Objective: The somatostatin-secreting delta cells in the islets of Langerhans appear to be regulated by neural mechanisms that have not been defined clearly. In this study, the celiac neural bundle of the human pancreas was electrically stimulated in the presence and absence of selective neural antagonists. Summary Background Data: The authors previously reported on studies of the splanchnic neural regulation of insulin, glucagon, and pancreatic polypeptide secretion. In these studies, alpha-adrenergic fibers appeared to have a predominant effect, strongly inhibiting the secretion of insulin, glucagon, and pancreatic polypeptide secretion. Cholinergic fibers appeared to stimulate strongly, although beta-adrenergic fibers weakly stimulated, the secretion of these hormones. Investigations of neural regulatory mechanisms governing human somatostatin release in vitro have not been previously reported. Methods: Pancreata were obtained from eight cadaveric organ donors. The isolated perfused human pancreas technique was used to assess the regulation of somatostatin secretion by the various neural fibers contained within the celiac plexus. The secretory response of somatostatin was examined in the presence of 16.7 mmol/L glucose, with and without neural stimulation, and specific neural antagonists. Results: The basal somatostatin secretion was 88 ± 26 fmol/g/min and increased 131 ± 23% (n = 8, p <0.01) in response to 16.7 mmol/L glucose. The augmentation seen with glucose was inhibited 66 ± 22% (n = 8, p <0.05) during celiac neural bundle stimulation. Alpha-adrenergic blockade resulted in a 90 ± 30% (n = 6, p <0.01) augmentation of somatostatin release. Beta-adrenergic blockade caused a 13 ± 2% (n = 6, p <0.05) suppression of somatostatin release. Complete adrenergic blockade resulted in a 25 ± 23% (n = 5, p = not significant) inhibition of somatostatin release. Cholinergic blockade resulted in a 40 ± 10% (n = 6, p <0.02) suppression of somatostatin release. Conclusions: The predominant effect of celiac neural bundle stimulation was inhibition of somatostatin secretion through an alpha- adrenergic effect. Beta-adrenergic fibers stimulate somatostatin secretion; cholinergic fibers have a negligible effect on somatostatin secretion. These data suggest that the splanchnic innervation of the pancreas has a potent regulatory role in somatostatin release in this in vitro human model.

AB - Objective: The somatostatin-secreting delta cells in the islets of Langerhans appear to be regulated by neural mechanisms that have not been defined clearly. In this study, the celiac neural bundle of the human pancreas was electrically stimulated in the presence and absence of selective neural antagonists. Summary Background Data: The authors previously reported on studies of the splanchnic neural regulation of insulin, glucagon, and pancreatic polypeptide secretion. In these studies, alpha-adrenergic fibers appeared to have a predominant effect, strongly inhibiting the secretion of insulin, glucagon, and pancreatic polypeptide secretion. Cholinergic fibers appeared to stimulate strongly, although beta-adrenergic fibers weakly stimulated, the secretion of these hormones. Investigations of neural regulatory mechanisms governing human somatostatin release in vitro have not been previously reported. Methods: Pancreata were obtained from eight cadaveric organ donors. The isolated perfused human pancreas technique was used to assess the regulation of somatostatin secretion by the various neural fibers contained within the celiac plexus. The secretory response of somatostatin was examined in the presence of 16.7 mmol/L glucose, with and without neural stimulation, and specific neural antagonists. Results: The basal somatostatin secretion was 88 ± 26 fmol/g/min and increased 131 ± 23% (n = 8, p <0.01) in response to 16.7 mmol/L glucose. The augmentation seen with glucose was inhibited 66 ± 22% (n = 8, p <0.05) during celiac neural bundle stimulation. Alpha-adrenergic blockade resulted in a 90 ± 30% (n = 6, p <0.01) augmentation of somatostatin release. Beta-adrenergic blockade caused a 13 ± 2% (n = 6, p <0.05) suppression of somatostatin release. Complete adrenergic blockade resulted in a 25 ± 23% (n = 5, p = not significant) inhibition of somatostatin release. Cholinergic blockade resulted in a 40 ± 10% (n = 6, p <0.02) suppression of somatostatin release. Conclusions: The predominant effect of celiac neural bundle stimulation was inhibition of somatostatin secretion through an alpha- adrenergic effect. Beta-adrenergic fibers stimulate somatostatin secretion; cholinergic fibers have a negligible effect on somatostatin secretion. These data suggest that the splanchnic innervation of the pancreas has a potent regulatory role in somatostatin release in this in vitro human model.

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