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

Stadil, F.; Rehfeld, J. F.; Christiansen, P. M.; Kronborg, O

doi:10.1002/bjs.1800611106

Cited by 43 publications

(19 citation statements)

References 9 publications

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“…First, studies using insulin hypoglycemia as a vagal stimulant must be interpreted with caution because there is evidence that hypoglycemic gastrin release is nonvagal (8)(9)(10). For example, the gastrin response to hypoglycemia persists after a complete vagotomy (8,9). Second, meal studies that have been done with atropine (2-4) are not definitive because atropine reduces acid secretion, and the resulting higher antral pH would facilitate gastrin release in response to any stimulant.…”

Section: Introductionmentioning

confidence: 99%

Effect of Atropine on Vagal Release of Gastrin and Pancreatic Polypeptide

Feldman¹,

Richardson²,

Taylor³

et al. 1979

J. Clin. Invest.

132

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A B S T R A C T We studied the effect ofseveral doses of atropine on the serum gastrin and pancreatic polypeptide responses to vagal stimulation in healthy human subjects. Vagal stimulation was induced by sham feeding. To eliminate the effect of gastric acidity on gastrin release, gastric pH was held constant (pH 5) and acid secretion was measured by intragastric titration. Although a small dose of atropine (2.3 ,ug/kg) significantly inhibited the acid secretory response and completely abolished the pancreatic polypeptide response to sham feeding, this dose of atropine significantly enhanced the gastrin response. Higher atropine doses (7.0 and 21.0,g/kg) had effects on gastrin and pancreatic polypeptide release which were similar to the 2.3-pAg/kg dose. Atropine (0.78 and 2.3 ,ug/kg) without sham feeding significantly inhibited basal acid secretion and also led to significant increases in serum gastrin above basal levels. The gastrin response to sham feeding with 2.3 ug/kg atropine was significantly greater than the sum of the gastrin responses to sham feeding alone and to 2.3 ,ug/kg atropine alone, indicating potentiation ofvagal gastrin release by atropine. We conclude: (a) Unlike vagally mediated gastric acid secretion and pancreatic polypeptide release which can be blocked by atropine, vagal gastrin release is potentiated by atropine. This observation suggests the existence of a vagal-cholinergic pathway which normally (i.e., in the absence of atropine) inhibits gastrin release. (b) Because atropine (without sham feeding) increased basal gastrin levels, it is likely that the cholinergic pathway which inhibits gastrin release is active even when the vagus nerve is not stimulated by sham feeding.

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Section: Introductionmentioning

confidence: 99%

Effect of Atropine on Vagal Release of Gastrin and Pancreatic Polypeptide

Feldman¹,

Richardson²,

Taylor³

et al. 1979

J. Clin. Invest.

132

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“…Stadil and Rehfeld [42] found that the stability of the response did not seem to be influenced by postoperative observation time: patterns of response were similar 2 and 14 weeks postoperatively, and no tendency towards change with time was observed. Figure 3 shows gastrin profiles [38].…”

Section: Resultsmentioning

confidence: 99%

“…Our radioimmunoassay, carried out according to the method described by Stadil and R ehfeld [34], showed an interassay variance of 25°/o and in a intraassay variance of 20% [26,31,32,34,36]. Samples of peripheral venous blood were drawn from an indwelling venous catheter at 15-min intervals throughout the examination.…”

Section: Radioimmunoassay Of Gastrinmentioning

confidence: 99%

The Place of Gastrin Determination in Ulcer Surgery

Säuberli¹

1976

Eur Surg Res

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This paper is concerned with the place of gastrin determination in ulcer surgery. Only the acid-stimulating properties of gastrin are considered. The role of the vagus in the gastrin response to a test meal was investigated in patients with duodenal ulcer. 50 patients were studied before and 3, 6 and 12 months after highly selective vagotomy without (25 patients) and with Wangensteen-pyloroplasty (25 patients). Basal and stimulated gastrin concentrations in serum, as determined by radioimmunoassay, were higher 3 months after the operation and 3 h after the test meal gastrin levels were still 50% higher than the basal levels. No difference was found between the patients treated with highly selective vagotomy and the patients treated with HSV and additional pyloroplasty. 6 and 12 months after the operation a moderate decrease of gastrin secretion was observed, but basal as well as stimulated levels were still elevated after 12 months compared to the values before operation. Our results indicate that the pattern of gastrin secretion changes as time passes after highly selective vagotomy with or without additional pyloroplasty.

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“…Enhanced gastrin responses to a test meal were observed only in about half the diabetic patients with vagal neuropathy and in the other patients, the same degree of response as seen in normal subjects and diabetic patients without vagal neuropathy. In patients with peptic ulcer, hypergastrinaemia is often detected not only after truncal vagotomy but also after selective proximal vagotomy [14][15][16]. The vagal inhibitory pathway for gastrin release may be located in the proximal stomach [14].…”

Section: Discussionmentioning

confidence: 99%

Augmented gastrin responses in diabetic patients with vagal neuropathy

Kanatsuka

Osegawa

et al. 1984

Diabetologia

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Summary.We evaluated serum gastrin responses to a test meal in normal subjects and diabetic patients with or without vagal neuropathy. Vagal neuropathy was defined as a heart rate variation during deep breathing of < 9 beats/min. Forty-three percent (54 out of 124) of the diabetic patients had abnormal heart rate variation, compared with 5% (3 out of 53) of the normal subjects. Serum gastrin responses to a test meal were examined in 17 normal subjects, 20 out of 70 diabetic patients without vagal neuropathy and 17 out of 54 diabetic patients with vagal neuropathy. Meal-stimulated gastrin levels were significantly higher in the diabetic patients with vagal neuropathy than in the normal subjects, while the findings in the diabetic patients without vagal neuropathy were similar to those in normal subjects, These data suggest that augmented gastrin responses are due to vagal denervation induced by autonomic neuropathy.

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

Cited by 43 publications

References 9 publications

Effect of Atropine on Vagal Release of Gastrin and Pancreatic Polypeptide

Effect of Atropine on Vagal Release of Gastrin and Pancreatic Polypeptide

The Place of Gastrin Determination in Ulcer Surgery

Augmented gastrin responses in diabetic patients with vagal neuropathy

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