Gastric secretory and plasma hormonal responses to sham-feeding of varying duration in patients with duodenal ulcer.

Konturek, Stanisław J.; Swierczek, J; Kwiecień, N; Obtutowicz, W; Dobrzańska, M.; Kopp, B; Oleksy, J

doi:10.1136/gut.22.12.1003

Cited by 47 publications

(27 citation statements)

References 21 publications

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“…These results are in accord with others' reports (Adrian et al 1979;Feldman et al 1979;Schwartz et al 1979;Konturek et al 1980Konturek et al , 1981. They demonstrate that vagal pathways play an important role, both in the basal state and the MSF-stimulated state, for the release of PP and that the mechanism of release is different between gastrin and PP.…”

Section: Discussionsupporting

confidence: 74%

“…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: 68%

“…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. Also it has been already reported that atropine produces enhancement rather than inhibition of gastrin release in response to MSF in duodenal ulcer patients (Konturek et al 1978(Konturek et al , 1980(Konturek et al , 1981 and healthy volunteers (Feldman et al 1979;Feldman and Walsh 1980). However, others could not find an increase in gastrin release.…”

Section: Discussionmentioning

confidence: 99%

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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: Discussionsupporting

confidence: 74%

Section: Discussionmentioning

confidence: 68%

Section: Discussionmentioning

confidence: 99%

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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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“…Duodenal ulcer healing by drugs that act by mechanisms other than H2-receptor blockade may produce lower relapse rates [3,6], Pirenzepine is a selective anti-muscarinic drug which reduces gastric secretion [7][8][9], and has been shown to accelerate the healing of duodenal ulcers [10][11][12], It has been shown to reduce the relapse rate of duodenal ulceration over a 1-year maintenance period when comparison was made with a placebo [13]. In comparison with cimetidine.…”

Section: Discussionmentioning

confidence: 99%

Comparison of Cimetidine and Pirenzepine in the Healing and Maintenance of Remission in Duodenal Ulcer

Gent

Hellier²

1990

Digestion

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The effect of cimetidine and pirenzepine on the maintenance of healing in duodenal ulceration has been compared in a multi-centre, controlled study. One hundred and sixty-six patients with endoscopically proven duodenal ulceration have been randomised to receive either cimetidine 200 mg t.i.d. and 400 mg nocte, or pirenzepine 50 mg b.i.d. for 6 weeks. Patients in each group were well matched for age, sex, weight and cigarette, alcohol and antacid consumption. After 6 weeks significantly more cimetidine-treated patients had healed ulcers: cimetidine showed 8 unhealed out of 79, and pirenzepine 19 out of 74 (p = 0.01). The follow-up phase lasted for 52 weeks or until patient withdrawal or ulcer relapse. During the follow-up phase 77.6% of cimetidine-treated and 68.8% of pirenzepine-treated patients relapsed. This difference in relapse rates is not statistically significant (p = 0.23).

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“…In previous studies the administration of piren zepine was found to cause a decrease in the PP response to sham feeding [3], but not to intravenous arginine [4], whereas a small but nonsignificant decrease in the response to a meal was observed [5]. This suggests that at least some of the stimulating effects on PP were mediated through cholinergic M|-receptors.…”

mentioning

confidence: 98%

Cholinergic Regulation of PP Release Is Mediated through Muscarinic M<sub>1</sub>-Receptors

Kleibeuker

Jansen

1989

Digestion

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The effects of the selective muscarinic M₁-receptor antagonist pirenzepine and the nonselective muscarinic antagonist atropine on bombesin- and peptone-stimulated release of pancreatic polypeptide (PP) were studied in healthy subjects. To exclude any effect of changes in intraduodenal pH continuous intragastric titration was performed during all tests. Both pirenzepine (i.v. bolus 0.6 mg/kg) and atropine (i.v. bolus 15 μg/kg, followed by an infusion of 5 μg/kg·h) significantly reduced peptone-induced integrated mean rise of plasma PP from 28 ± 5 to 8 ± 4 and -2 ± 5 pmol/l, respectively (n = 4). Both drugs also reduced bombesin-induced rise of plasma PP in all 4 subjects, from 27 ± 12 to 6 ± 4 and 7 ± 1 pmol/l (0.05 < p < 0.1). It is concluded that cholinergic regulation of PP release is mediated mainly through muscarinic M₁-receptors.

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Gastric secretory and plasma hormonal responses to sham-feeding of varying duration in patients with duodenal ulcer.

Cited by 47 publications

References 21 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.

Comparison of Cimetidine and Pirenzepine in the Healing and Maintenance of Remission in Duodenal Ulcer

Cholinergic Regulation of PP Release Is Mediated through Muscarinic M<sub>1</sub>-Receptors

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