Effect of proximal gastric vagotomy and anticholinergics on the acid and gastrin responses to sham feeding in duodenal ulcer patients.

Stenquist, Bo; Rehfeld, J. F.; Olbe, L

doi:10.1136/gut.20.11.1020

Cited by 29 publications

(8 citation statements)

References 30 publications

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“…They found a significant rise of serum gastrin level during MSF, either in the case of simple aspiration of gastric juice or maintaining the gastric content at pH 5.0 by intragastric titration. Stenquist et al (1979) reported, however, no significant rise of plasma gastrin without using the intragastric titration technique like in our study. These discrepancies are difficult to explain, but may be due to differences in doses of atropine, sham feeding technique and with or without the use of intragastric titration.…”

Section: Discussioncontrasting

confidence: 42%

“…Konturek et al (1978Konturek et al ( , 1980Konturek et al ( , 1981 and Stenquist et al (1979) did not find an increase of plasma gastrin concentration after sham feeding, while Feldman et al (1979) and Feldman and Walsh (1980) reported contrary. They found a significant rise of serum gastrin level during MSF, either in the case of simple aspiration of gastric juice or maintaining the gastric content at pH 5.0 by intragastric titration.…”

Section: Discussionmentioning

confidence: 70%

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Plasma gastrin and pancreatic polypeptide response to atropine and sham feeding in man.

Koizumi

Ushizawa

Kawamura

et al. 1984

Tohoku J. Exp. Med.

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We studied the effects of atropine, both in the basal state and after stimulation by modified sham feeding (MSF), and the effect of MSF alone, on the plasma gastrin and pancreatic polypeptide (PP) responses in 8 healthy human subjects. Atropine 1 mg in the basal state had no effect on the plasma gastrin concentrations but led to significant decrease in plasma PP concentrations. Plasma gastrin response to MSF was negligible but increased by atropine. The plasma PP level was markedly increased by MSF, and was antagonized by atropine. This study shows that the release of plasma PP during basal state and after MSF is under the control of the vagalcholinergic mechanism, but plasma gastrin is controlled by a different mechanism.gastrin ; pancreatic polypeptide ; atropine ; sham feedingEffects of atropine on plasma gastrin in man in the basal level and in the vagally mediated stimulation have been reported by several authors but are still a subject of controversy. On the other hand, PP is a recently characterized 36 amino acid peptide, discovered by Kimmel et al. (1968) and by Lin and Chance (1974) independently.But the release mechanism involving cephalic phase of plasma PP has not been elucidated in detail as yet. The purpose of the present study was to evaluate the effect of vagal stimulation archieved by sham feeding and the effect of the cholinergic blockade, atropine, on the gastrin and PP response both in the basal state and after stimulation by sham feeding in man. MATERIALS AND METHODSEight healthy volunteers (mean age 21 years, range 20-23 years) free from gastrointestinal disease participated as subjects in this study. On separate test days, three series of tests (A, B, C) were performed in random order after overnight fast on each subject.A. Effect of atropine during the basal state. After a 120-min control period, 1 mg of atropine sulfate (Tanabe, Osaka) was injected intramuscularly. Blood samples were taken

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Section: Discussioncontrasting

confidence: 42%

Section: Discussionmentioning

confidence: 70%

Plasma gastrin and pancreatic polypeptide response to atropine and sham feeding in man.

Koizumi

Ushizawa

Kawamura

et al. 1984

Tohoku J. Exp. Med.

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“…Modified sham feeding seems to adequately reflect normal physiological vagal activation of gastric secretion (18), which was confirmed by the observation that complete vagotomy abolished the acid response to sham feeding (19,20). The pathological mechanisms of stress ulceration nave otten been attnbuted to gastric hypersecretion (21)(22)(23).…”

Section: Discussionmentioning

confidence: 72%

GABAA and GABAB-receptor agonists evoked vagal nerve efferent transmission in the rat.

Yamasaki

Gotō

Hara³

et al. 1991

Jpn.J.Pharmacol

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ABSTRACT-The effect of GABA agonists on vagal efferent activity was studied in anesthetized rats. PCPGABA, a GABAB agonist (4 and 8 mg/kg, s.c.), markedly activated the neural efferent discharge of the vagus. Muscimol, a GABAA agonist (0.1 and 0.3 mg/kg, i.v.), also facilitated vagal activity. Both agonists caused significant gastric acid hyperacidity. Bicuculline (0.25 mg/kg, i.v.) or picrotoxin (0.5 mg/kg, i.v.) given 10 min prior to each agonist had no effect on the frequency of vagal nerve firing elicited by PCPGABA (4 mg/kg, s.c.) or muscimol (0.3 mg/kg, i.v.). Pretreatment with scopolamine (0.25 mg/kg, i.v.) abolished PCPGABA stimulated vagal activity and gastric acid secretion. Methscopolamine (0.25 mg/kg, i.v.) inhibited only the hyperacidity evoked by PCPGABA, but not vagal activation. These results suggest that PCPGABA and muscimol may cause gastric acid secretion through central cholinergic descending mechanisms that are resistant to GABAA and GABAB antagonists.

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“…This antimuscarinic drug was chosen since it is known not to pass the blood-brain barrier. The larger dose used has previously been shown to inhibit the acid response to shamfeeding in man by about 65%, whereas a further increase in dose did not induce a more profound inhibition [4]. A 10 times lower dose of benzilonium bromide was also investi gated in view of the previously obtained results with low doses of atropine [4,5], indicating a susceptibility of inhibitory vagal fibers to even minute amounts of an antimuscarinic substance.…”

Section: Patientsmentioning

confidence: 99%

“…In man physiological vagal stimulation has been re ported to induce a small but significant gas trin response [2,3], whereas others have ex perienced difficulties in demonstrating any effect [4], In this context it seems relevant to point out that the vagus nerve exerts a dual action on the gastrin cells in the antrum, the most predominant one being of inhibitory nature [2. 5, 6], In addition, experiments in dogs have also suggested an inhibitory mech anism operating on the gastrin cells at least partly via local nervous reflexes from the fundic region [7], suggesting complex ner vous control of gastrin secretion.…”

mentioning

confidence: 99%

Effect of Parietal Cell Vagotomy and Cholinergic Blockade on Gastrin Release in Man Induced by Gastrin-Releasing Peptide

Sjövall¹,

Lindstedt

Olbe³

et al. 1990

Digestion

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The influence of cholinergic blockade as well as vagal denervation of the oxyntic gland mucosa on the gastrin response to gastrin-releasing peptide (GRP) have been studied in patients with duodenal ulcer disease. The gastric luminal content was neutralized during the experiments. GRP induced a substantial increase in gastrin levels with a peak response already after 15 min of infusion. Vagal denervation of the parietal cell area induced a significant increase in basal gastrin concentrations and a significant enhancement of the GRP response. Two different doses of benzilonium bromide were studied and neither influenced the basal concentrations of gastrin. A significantly increased gastrin response to GRP was, however, observed after administration of both a high and a very low dose of the anticholinergic drug. Our results delineate a vagal, noncholinergic inhibitory influence on the basal gastrin release. In addition a vagally dependent oxyntopyloric mechanism inhibits the gastrin release stimulated by GRP. This inhibitory mechanism may hypothetically be a cholinergic reflex mechanism.

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Effect of proximal gastric vagotomy and anticholinergics on the acid and gastrin responses to sham feeding in duodenal ulcer patients.

Abstract: SUMMARY Plasma gastrin concentrations and gastric acid output after modified sham feeding were determined in 20 duodenal ulcer patients. Sham

Cited by 29 publications

References 30 publications

Plasma gastrin and pancreatic polypeptide response to atropine and sham feeding in man.

Plasma gastrin and pancreatic polypeptide response to atropine and sham feeding in man.

GABAA and GABAB-receptor agonists evoked vagal nerve efferent transmission in the rat.

Effect of Parietal Cell Vagotomy and Cholinergic Blockade on Gastrin Release in Man Induced by Gastrin-Releasing Peptide

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