Sympathetic activation: a mechanism for morphine induced pain and rises in liver enzymes after cholecystectomy?

Ic, Roberts-Thomson; Jonsson, Julie R.; Frewin, D. B.; Coates, G.

doi:10.1136/gut.31.2.217

Cited by 7 publications

(5 citation statements)

References 20 publications

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“…In this respect, the mechanism of pain with CCK-8 appears to differ from that with morphine, where sympathetic activation not only accompanies the development of pain but may precede the onset of pain. 7 Since the digestion products of fat and protein in the proximal small bowel are major stimuli to endogenous CCK secretion: the above results could explain the high frequency of fat intolerance in patients with various functional bowel syndromes. Furthermore, improvement in symptoms may follow a reduction in dietary fat andor the use of novel agents such as devazepide which antagonize the effects of CCK on CCKA receptomZ0 ,…”

Section: Discussionmentioning

confidence: 99%

Responses to cholecystokinin octapeptide in patients with functional abdominal pain syndromes

Roberts‐Thomson

Fettman

Jonsson

et al. 1992

J of Gastro and Hepatol

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Clues to the pathogenesis of functional pain syndromes may be derived from the study of stimuli that precipitate or aggravate symptoms. In this study, cholecystokinin octapeptide (CCK-8, 0.06 microgram/kg) and placebo were given by intravenous infusion (5 min) in random order to control subjects and four groups of patients with unexplained abdominal pain. Induction of pain and nausea were assessed by linear analogue scales while sympathoadrenomedullary responses were assessed by serial changes in plasma concentrations of noradrenaline, adrenaline and dopamine. Scores for pain and nausea were low after infusion of placebo. After infusion of CCK-8, pain scores were significantly higher in patients with spontaneous pain than in control subjects, but significant increases in nausea were restricted to patients with irritable bowel syndrome and a subgroup of patients with pain after cholecystectomy. Although some groups showed increases in plasma concentrations of catecholamines after the infusion of CCK-8, the size of these increases was neither consistent among patients within each group nor predictive of scores of pain and nausea in individual subjects. Pain during the infusion of CCK-8 was a feature common to patients with diverse functional pain syndromes, and did not appear to be attributable to activation of the sympathetic nervous system.

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Section: Discussionmentioning

confidence: 99%

Responses to cholecystokinin octapeptide in patients with functional abdominal pain syndromes

Roberts‐Thomson

Fettman

Jonsson

et al. 1992

J of Gastro and Hepatol

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“…Autonomic dysregulation has also been proposed as the cause of the motility disorder. Sympathetic overactivity has been found under basal conditions and during pain episodes in patients with postcholecystectomy pain who develop pain in association with morphine administration (53,54). Furthermore, the severity of the pain in this patient group can be attenuated by clonidine (55), a sympathetic antagonist.…”

Section: Mechanism Of So Dysfunctionmentioning

confidence: 99%

Sphincter of Oddi Function and Dysfunction

Toouli

Craig²

2000

Canadian Journal of Gastroenterology

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The sphincter of Oddi (SO) is situated at the junction of the bile and pancreatic ducts where they enter the duodenum, and it serves to regulate the flow of bile and pancreatic juices as well as to prevent the reflux of duodenal contents into the pancreatobiliary system. SO dysfunction relates to either the biliary or pancreatic portions of the sphincter. Distinct clinical syndromes relating to either sphincter segment are recognized. The mechanism of dysfunction remains uncertain, but disruption of neural pathways involved in sphincter function seems likely. SO dysfunction is best diagnosed by manometry, which is able to correctly stratify patient groups and determine therapy. Biliary scintigraphy, which is noninvasive, has shown promise as a screening tool for patients with suspected SO dysfunction. Division of the sphincter is an effective treatment for patients with manometrically proven SO stenosis for either the biliary or pancreatic form of the disorder. Other forms of SO dysfunction may benefit from pharmacotherapy.

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“…Major trauma and severe injury result in post‐trauma stress disorder, which activates the sympathetic system and induces a catecholamine surge . In turn, this pathophysiologic reaction leads to host damage by activating adrenergic β‐receptors.…”

Section: Introductionmentioning

confidence: 99%

“…Major trauma and severe injury result in post-trauma stress disorder, which activates the sympathetic system and induces a catecholamine surge. [3][4][5][6] In turn, this pathophysiologic reaction leads to host damage by activating adrenergic β-receptors. 7,8 Recently, a growing body of research has revealed that activation of β-receptors negatively modulates bone remodelling under physiological conditions 9,10 and impairs bone metabolism and bone fracture healing after trauma.…”

mentioning

confidence: 99%

Blockade of adrenergic β‐receptor activation through local delivery of propranolol from a 3D collagen/polyvinyl alcohol/hydroxyapatite scaffold promotes bone repair in vivo

Song

et al. 2019

Cell Proliferation

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Objectives Activation of the sympathetic system and adrenergic β‐receptors following traumatic bone defects negatively impairs bone regeneration. Whether preventing β‐receptor activation could potentially improve bone defect repair is unknown. In this study, we investigated the effect of systematic administration and local delivery of propranolol through composite scaffolds on bone healing. Materials and methods Collagen/PVA/propranolol/hydroxyapatite（CPPH）composite scaffolds were fabricated with 3D printing technique and characterized by scanning electron microscope (SEM). Micro‐CT analysis and bone formation histology were performed to detect new bone formation. Osteogenic differentiation of bone marrow stromal cells (BMSCs) and osteoclastogenesis of bone marrow monocytes cultured with scaffolds extract were performed for further verification. Results Intraperitoneal injection of propranolol did not significantly improve bone repair, as indicated by micro‐CT analysis and bone formation histology. However, CPPH scaffolds exhibited sustained release of propranolol in vitro and significantly enhanced bone regeneration compared with vehicle collagen/PVA/hydroxyapatite (CPH) scaffolds in vivo. Moreover, in vitro experiments indicated the scaffolds containing propranolol promoted the osteogenic differentiation and migration of rat BMSCs and inhibited osteoclastogenesis by preventing β‐receptor activation. Conclusions This study demonstrates that local adrenergic β‐receptor blockade can effectively enhance the treatment of bone defects by stimulating osteogenic differentiation, inhibiting osteoclastogenesis and enhancing BMSCs migration.

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Sympathetic activation: a mechanism for morphine induced pain and rises in liver enzymes after cholecystectomy?

Cited by 7 publications

References 20 publications

Responses to cholecystokinin octapeptide in patients with functional abdominal pain syndromes

Responses to cholecystokinin octapeptide in patients with functional abdominal pain syndromes

Sphincter of Oddi Function and Dysfunction

Blockade of adrenergic β‐receptor activation through local delivery of propranolol from a 3D collagen/polyvinyl alcohol/hydroxyapatite scaffold promotes bone repair in vivo

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