Effect of proximal gastric vagotomy on gastric acid secretion and plasma gastrin

Clark, C. G.; Lewin, M. R.; Stagg, B. H.; Wyllie, J. H.

doi:10.1136/gut.14.4.293

Cited by 24 publications

(5 citation statements)

References 12 publications

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“…Two patients were excluded owing to difficulties in interpreting the data from the insulin test, patients serve as their own control when influences of different treatments on gastrin release by food are studied. This has, to our knowledge, only been done in one previous study of patients with highly selective vagotomy (Clark et al, 1973). Two groups have previously reported studies on gastrin responses to feeding after SV and HSV (Jaffe et al, 1972;Hansky and Korman, 1973).…”

Section: 05mentioning

confidence: 94%

“…No exact figures were given, but the main difference seemed to be higher concentrations in the early phase of stimulation. Clark et al (1973) reported a decrease in the gastrin responses to meat extract after HSV in 8 patients with a negative Hollander response t o insulin. In contrast, the mean gastrin response was unchanged postoperatively in 8 patients with a 'positive insulin test'.…”

Section: 05mentioning

confidence: 99%

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Gastrin response to food in duodenal ulcer patients before and after selective or highly selective vagotomy

Stadil

Rehfeld

Christiansen

et al. 1974

Journal of British Surgery

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The role of the vagus in the gastrin response to a steak meal was investigated in patients with duodenal ulcer. Thirty patients were studied before and after vagal denervationoftheentire stomach (selective vagotomy and pyloroplasty). Basal and stimulated gastrin concentrations in serum, as determined by radio-immunoassay, were higher postoperatively (87 pre-/I I1 postopera- tively (basal) and 2431341 (peak) pglml). Thirty other patients were studied before and afier denervation of the gastric body (highly selective vagotomy). Bnsnl and stimulated gastrin concentrations were also higher postoperatively in these patients (941133 and 2771343 pglml respectively). The differences between the two groups were insignifcant. Between individuals, gastrin responses varied markedly, but pre-and postoperative responses were positively related within the same subject. No differences were observed between patients with 'positive' or 'negative' Hollander responses to insulin. In 6 subjects studied 2 and 14 weeks postoperatively no difierenre was apparent between the two studies.It is concluded that antral branches of the uagi play only a minor role, if any, in the gastrin response to food.

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Section: 05mentioning

confidence: 94%

Section: 05mentioning

confidence: 99%

Gastrin response to food in duodenal ulcer patients before and after selective or highly selective vagotomy

Stadil

Rehfeld

Christiansen

et al. 1974

Journal of British Surgery

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“…However, the results were inconsistent, with some studies reporting a decrease in weight and others reporting no difference or even an increase in weight . Furthermore, a vagotomy also reduces gastric relaxation, motility and secretions, that is, acid and gastrin, all making a role for the vagus in the control of food intake hard to identify. Perivagal application of capsaicin has also been used to specifically destroy vagal afferent fibers .…”

Section: The Importance Of the Vagus In Food Intake Regulationmentioning

confidence: 99%

Plasticity of gastrointestinal vagal afferent satiety signals

Page

Kentish

2016

Neurogastroenterology Motil

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The vagal link between the gastrointestinal tract and the central nervous system (CNS) has numerous vital functions for maintaining homeostasis. The regulation of energy balance is one which is attracting more and more attention due to the potential for exploiting peripheral hormonal targets as treatments for conditions such as obesity. While physiologically, this system is well tuned and demonstrated to be effective in the regulation of both local function and promoting/terminating food intake the neural connection represents a susceptible pathway for disruption in various disease states. Numerous studies have revealed that obesity in particularly is associated with an array of modifications in vagal afferent function from changes in expression of signaling molecules to altered activation mechanics. In general, these changes in vagal afferent function in obesity further promote food intake instead of the more desirable reduction in food intake. It is essential to gain a comprehensive understanding of the mechanisms responsible for these detrimental effects before we can establish more effective pharmacotherapies or lifestyle strategies for the treatment of obesity and the maintenance of weight loss.

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“…), secretion and motility (Clark et al . ; Tanaka et al . ), is coordinated and regulated with behavioural responses, such as food intake (Gil et al .…”

Section: Introductionmentioning

confidence: 99%

“…Vagal afferents are extensively distributed in the upper GI tract. These sensory nerves project to the central nervous system (CNS) where gut reflex function, such as gastric accommodation (Takasugi et al 1982), secretion and motility (Clark et al 1973;Tanaka et al 2001), is coordinated and regulated with behavioural responses, such as food intake (Gil et al 2011). Therefore many of the actions of NO within the GI tract could be via modulation of these vagally mediated responses.…”

Section: Introductionmentioning

confidence: 99%

Diet‐dependent modulation of gastro‐oesphageal vagal afferent mechanosensitivity by endogenous nitric oxide

Kentish

O’Donnell

Wittert

et al. 2014

The Journal of Physiology

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Key pointsr Nitric oxide (NO) is an important signalling molecule found in the gastrointestinal tract, which can modulate the mechanosensitivity of gastro-oesophageal vagal afferents.r It is known that the effects of NO on food intake depend on feeding status, but the effect of NO on gastro-oesophageal vagal afferents in different feeding conditions is unknown.r We show that in the fed state endogenous NO inhibits mucosal afferents through a pathway involving nicotinamide adenine dinucleotide phosphate (NADPH) oxidase.r In mice fasted overnight endogenous NO potentiates the response of mucosal strokingand tension-sensitive afferents to mechanical stimuli via a mechanism involving hyperpolarisation-activated cyclic nucleotide-gated 3 (HCN3) channels.r These results show the role of NO in the peripheral modulation of gastro-oesophageal vagal afferents is dynamic and dependent on feeding status.Abstract Neuronal nitric oxide (NO) plays an important role in gastric motor activity and modulates the mechanosensitivity of gastro-oesophageal vagal afferents. Effects of NO on food intake are dependent on feeding status. We sought to determine the effect of NO on gastro-oesophageal vagal afferent activity in the normally fed and food-restricted states and the second messenger pathways mediating these effects. Eight week old female C56BL/6 mice were fed ad libitum or food restricted for 14 h. An in vitro preparation was used to determine the functional effects of NO and the second messenger pathways involved. Expression of NO signal transduction molecules in vagal afferents was determined by reverse-transcription polymerase chain reaction (RT-PCR). Endogenous NO and the NO donor S-nitroso-N-acetylpenicillamine (SNAP) inhibited vagal mucosal afferent responses to tactile stimuli in mice fed ad libitum. After a 14 h fast endogenous NO and SNAP potentiated tension and mucosal afferent responses to mechanical stimulation. The excitatory effect of NO was blocked by the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor apocynin. After a 14 h fast expression of NADPH oxidase 2 (NOX2) mRNA in whole nodose ganglia was significantly reduced and the excitatory effect of NO on gastro-oesophageal vagal afferents was lost. Under fasting conditions the inhibitory effect of NO was blocked with the hyperpolarisation-activated cyclic nucleotide-gated (HCN) channel blocker ivabradine and mRNA expression of HCN3 in the nodose ganglia was elevated. In conclusion, the role of NO in the peripheral modulation of gastro-oesophageal vagal afferents is dynamic and dependent on feeding status.

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Effect of proximal gastric vagotomy on gastric acid secretion and plasma gastrin

Cited by 24 publications

References 12 publications

Gastrin response to food in duodenal ulcer patients before and after selective or highly selective vagotomy

Gastrin response to food in duodenal ulcer patients before and after selective or highly selective vagotomy

Plasticity of gastrointestinal vagal afferent satiety signals

Diet‐dependent modulation of gastro‐oesphageal vagal afferent mechanosensitivity by endogenous nitric oxide

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