Propranolol and Serum Gastrin in Postvagotomy Insulin Tests

Hall, William H.; Durkin, Martin G.; Read, Raymond C.

doi:10.1159/000197458

Cited by 9 publications

(3 citation statements)

References 5 publications

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“…The clear rise shown here during hypoglycaemia preceded by atropine is similar to the findings of Farooq and Walsh (1975) and supports that of others who have found that vagotomy (Stadil, 1972;Hall et al, 1973) or vagal cooling (Cairns et al, 1974) did not inhibit the gastrin response. We cannot totally exclude, however, that the enhanced gastrin response may be related to a lesser degree of acidinhibition of gastrin release found after atropine.…”

Section: Discussionsupporting

confidence: 92%

Role of neural influences in the release of gastrin, glucagon, and secretin during hypoglycaemia in man.

McLoughlin¹,

Hayes²,

Buchanan³

et al. 1978

Gut

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BelfastSUMMARY Both vagal and sympathetic innervation been have described as influencing hormone release from the gastrointestinal tract and pancreas. The role of neural influences on the release of gastrin, glucagon, and secretin has been studied using the potent autonomic nerve stimulus of hypoglycaemia. Healthy subjects were each rendered hypoglycaemic by insulin 0-2 units/kg on three occasions: after atropine 20 pg/kg: after propranolol 160 mg orally, and without prior drug administration.Adequate beta-blockade was confirmed by observation of the pulse rate response to a standard exercise at the end of the experiment, and by measurement of plasma propranolol levels. Hypoglycaemia failed to produce a rise in plasma gastrin under either propranolol or control conditions but a significant rise was noted with prior atropinisation. The glucagon response to hypoglycaemia, when measured with either the C-or N-terminal reactive antibodies, was found not to be influenced to any significant extent by either beta-blockade or atropinisation. No alteration in plasma secretin levels was noted during hypoglycaemia. It therefore appears that neural influences are relatively unimportant in the release of gastrin, glucagon, and secretin in man.

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Section: Discussionsupporting

confidence: 92%

Role of neural influences in the release of gastrin, glucagon, and secretin during hypoglycaemia in man.

McLoughlin¹,

Hayes²,

Buchanan³

et al. 1978

Gut

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show abstract

“…Contradictory findings of previous authors, who had reported an unchanged gastrin response to insulin after 20 mg propranolol given orally, must be related to the different dosage and the route of administration of the drug (2,5). A single oral dose of propranolol below 30 mg is completely extracted from the liver by high tissue affinity binding (8).…”

Section: Discussionmentioning

confidence: 94%

Serum Gastrin Concentration after Sham Feeding and Feeding under the Influence of Propranolol in Man

Kaess¹,

Fanger²,

Teckentrup³

et al. 1976

Digestion

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The influence of propranolol, 50 μg/kg administered intravenously, on the gastrin concentration during sham feeding and after a test meal was studied in eight normal subjects. β-Adrenergic blockade had no inhibitory effect on the gastrin response to feeding. Sham feeding did not provoke a significant rise of serum gastrin concentration; however, in three subjects a definite gastrin response occurred in the presence of β-adrenergic blockade.

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“…This finding is contrary to the opinion that blood-borne adren aline should play a role in the production of gastric acid in man. Such a hypothesis has emerged from previous investigations demon strating that propranol pre-treatment can re duce acid secretion by up to 60% (8,12) and that infusions of adrenaline -but not nor adrenaline stimulate acid output (5). Again, it remains to be shown whether these results are due to pharmacological effects, central or otherwise.…”

Section: Discussionmentioning

confidence: 99%

The Role of Catecholamines in the Control of Gastrin and Acid Secretion during Insulin Hypoglycaemia in Man

Järhult¹,

Hamberger²,

Lanthén³

et al. 1981

Digestion

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5 adrenalectomized subjects and 8 healthy volunteers underwent an insulin test during which acid secretion and plasma adrenaline, noradrenaline, dopamine and gastrin concentrations were measured. Plasma glucose concentration fell by > 50% in all subjects. The mean plasma adrenaline concentration increased markedly ( > 1,000%) in the normal group but was unchanged in the adrenalectomized group. In all subjects, plasma noradrenaline concentration increased moderately, whereas plasma dopamine levels remained unchanged. Clear-cut increments in plasma gastrin concentration were seen only in 3 participants, each of whom responded to insulin hypoglycaemia with an extremely high adrenaline release. Basal and peak acid output were similar in adrenalectomized and normal subjects. The results suggest that circulating catecholamines contribute to the control of gastrin and acid secretion in man only during circumstances with high plasma catecholamine levels, e.g. severe stress.

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Propranolol and Serum Gastrin in Postvagotomy Insulin Tests

Cited by 9 publications

References 5 publications

Role of neural influences in the release of gastrin, glucagon, and secretin during hypoglycaemia in man.

Role of neural influences in the release of gastrin, glucagon, and secretin during hypoglycaemia in man.

Serum Gastrin Concentration after Sham Feeding and Feeding under the Influence of Propranolol in Man

The Role of Catecholamines in the Control of Gastrin and Acid Secretion during Insulin Hypoglycaemia in Man

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