The effect of beta-adrenergic blockade upon basal and pentagastrin-stimulated gastric acid secretion and upon gastrin response to food.

Beta-adrenergic blockade with 10 mg of propanolol had no significant effect upon the spontaneous gastric acid secretion, while the maximum (pentagastrin) acid secretion was depressed in healthy subjects and patients with duodenal ulcer. The gastrin response to food was significantly higher during beta-adrenergic blockade. It is suggested that a minor part of the maximum acid secretion may be due to activation of beta-receptors, while the gastrin response to food is probably not related to activation of beta-receptors.     

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

Sixteen patients underwent proximal gastric vagotomy (highly selective vagotomy) for chronic duodenal ulceration. All were subjected to preoperative and postoperative acid secretion studies. A reduction in the secretory response to pentagastrin and abolition of the response to meat extract occurred postoperatively.Plasma gastrin levels in response to meat extract were studied by radioimmunoassay. Basal plasma gastrin levels were unaffected by vagotomy and it was found that the plasma gastrin response to meat extract was not impaired after operation if the postoperative insulin test was positive. Only if the insulin test was negative was the amount of gastrin released by meat extract reduced.     

Insulin-stimulated gastric acid secretion after vagotomy in man

The gastric acid response to insulin was studied in a group of patients who had had incomplete truncal vagotomies and in 22 patients with complete vagotomies. A dose-response study of gastric acid secretion after insulin in 17 patients with incomplete vagotomy indicated that a dose of 0.2 unit/kg was greatly superior to 0.4 unit/kg and marginally superior to 0.1 unit/kg in eliciting the highest acid response. Eight early responders had a significantly greater peak acid output after insulin, 0.2 unit/kg, than 9 late responders, but only 1 early responder developed a recurrent ulcer compared with 4 patients in the late group. The timing of a patient's positive Hollander response to insulin was not related to the optimum dose of insulin in that patient. The blood glucose response to insulin, 0.2 unit/kg, was unchanged after complete vagotomy. The changes of blood glucose after a given dose of insulin varied from one individual to another. This variation could account for the fact that the dose which produced highest peak acid output in some individuals was 0.1 unit/kg and in others 0.2 unit/kg.     

Fat inhibition of gastric acid secretion in duodenal ulcer patients before and after proximal gastric vagotomy.

In seven duodenal ulcer patients the effect of intraduodenal infusion of 20 ml oleic acid on submaximal gastric acid secretion stimulation by a continuous pentagastrin infusion was evaluated before and after proximal gastric vagotomy. In the control tests 20 ml of saline was given. Before vagotomy, oleic acid evoked a significant inhibition of gastric acid secretion of 25% compared with the controls. This inhibition was abolished after proximal gastric vagotomy. The difference in inhibition before and after vagotomy was significant (P=0.01). It is concluded that the vagus nerve in man plays a decisive role in duodenal fat inhibition of gastric acid secretion.     

Specific beta-adrenergic mechanisms in the hypoglycaemic activation of gastrin and gastric acid secretion

To study whether specific beta-adrenergic mechanisms contribute to the hypoglycaemic activation of gastrin and gastric acid secretion, the effects of racemic and dextroisomer propranolol (0.1 mg/kg, intravenously) were studied during insulin tests (0.2 IU/kg) in 13 persons. dl-Propranolol inhibited the gastrin response to hypoglycaemia markedly and more than the insignificant alteration observed after d-propranolol. Gastric acid response to hypoglycaemia was significantly reduced by dl-propranolol and not by d-propranolol. The findings demonstrate that non-beta-adrenergic effects of propranolol on the stomach are minor and that specific beta-adrenergic mechanisms are directly or indirectly involved in the hypoglycaemic stimulation of the stomach.     

Influence of beta blockade on gastric acid secretion and changes in gastric mucosal blood flow before and after parietal cell vagotomy in dogs and man

The aim of the present study was, in paired experiments in dogs, to examine the effect of beta-receptor blockade on gastric acid secretion and mucosal blood flow before and after parietal cell vagotomy (PCV). The secretory response to pentagastrin was reduced after vagotomy. beta-Adrenergic blockade had no effect on pentagastrin-stimulated gastric acid secretion before PCV, but after PCV beta blockade caused a modest increase in acid secretion, mediated mainly by the beta 2 receptors. A similar trend was seen in man. A marked increase in mucosal blood flow occurred 30 min after propranolol and was followed by a late decrease. One may conclude that a modest beta-adrenergic tone, which reduces secretion, becomes manifest after vagal denervation and that an increase in the ratio between mucosal blood flow and acid secretion was induced by the PCV. This increase cannot be explained as a beta-receptor-mediated effect.     

Relationship between insulin- and histamine-stimulated gastric secretion before and after vagotomy.

The relationship of gastric secretion in response to a single injection of insulin and in response to a histamine infusion, in unoperated patients with duodenal ulcer was studied before and after vagotomy. The secretion in response to insulin was significantly less than that in response to histamine. The ratio was about 0.7 before vagotomy, and about 0.4 after vagotomy irrespective of the adequacy of vagotomy. Highly significant correlations were obtained between the responses to the two stimuli, both in the unoperated group and in the whole postoperative group as well as in the inadequate vagotomy group, but not in patients after adequate vagotomy. Thus, the proportional differences between individuals in response to insulin were substantially the same as the proportional differences in response to histamine. The algebraic excess of histamine- over insulin-stimulated secretion before vagotomy did not differ from the value after vagotomy. Histamine-stimulated secretion after adequate vagotomy approximated to, but after inadequate vagotomy was greater than the preoperative algebraic excess of histamine- over insulin-stimulated secretion. These results are consistent with a new model of acetylcholine/histamine-receptor relationships. A certain proportion of the parietal cells are insensitive to the vagus but sensitive to histamine; and those sensitive to the vagus are also sensitive to histamine, but only when their vagal innervation is intact.     

Changes in gastric acid secretion assayed by endoscopic gastrin test before and after Helicobacter pylori eradication

BACKGROUND: It remains controversial whether or not Helicobacter pylori infection causes altered gastric acid secretion. A novel test for evaluating gastric acid secretion (endoscopic gastrin test; EGT) has recently been developed. AIM: To investigate by EGT the effects of H pylori eradication on the state of gastric acid secretion in patients with peptic ulcer. METHODS: Twenty six patients with duodenal ulcer and 33 with gastric ulcer, for all of whom H pylori infection had been documented, were studied by EGT, histological examination of gastric mucosa, and measurement of plasma gastrin levels before and one and seven months after H pylori eradication. RESULTS: In patients with duodenal ulcer, the mean EGT value before H pylori eradication was higher than that in H pylori negative controls, but it had decreased significantly seven months after the treatment. In contrast, the mean EGT value of patients with gastric ulcer before H pylori eradication was lower than that in H pylori negative controls, but it had increased one month after the treatment; this was followed by a slight decrease at seven months. In both groups, mean EGT values seven months after the treatment were not significantly different from the mean control value. CONCLUSIONS: The reduced acid secretion in gastric ulcer patients and gastric acid hypersecretion in duodenal ulcer patients were both normalised after the clearance of H pylori.     

The effect of retaining antral innervation on the reductions of gastric acid and pepsin secretion after vagotomy

The result of a prospective trial of 40 patients with duodenal ulcer treated either by proximal gastric vagotomy (antrum innervated) or by selective vagotomy (antrum denervated) shows that they are equally effective in reducing gastric acid and pepsin secretion.Preservation of antral innervation by proximal gastric vagotomy reduces gastric secretion as effectively as denervation of the entire stomach.     

Neurotensin induced inhibition of gastric acid secretion in duodenal ulcer patients before and after parietal cell vagotomy

The influence of the vagal nerve on the inhibitory effect of neurotensin on pentagastrin stimulated gastric acid secretion was investigated in seven duodenal ulcer patients before and after parietal cell vagotomy without drainage. Preoperatively, neurotensin inhibited gastric acid secretion, whereas no effect was found postoperatively. Plasma concentration of neurotensin was identical pre-and postoperatively. This study shows that the inhibitory effect of neurotensin on gastric acid secretion is dependent on an intact vagal innervation of the parietal cell area.     

The effect of calcium on gastric acid and gastrin secretion in antrectomized subjects

Serum gastrin concentrations and gastric acid secretion were measured in nine antrectomized subjects during infusion of saline and calcium gluconate. The basal gastrin level was of the same magnitude as in normal individuals and unoperated duodenal ulcer patients. Calcium infusion only induced gastrin release in one patient and did not induce acid secretion in any of the patients.