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Biomedical subjects

L Olbe

Publications and source records attributed to L Olbe.

At least 127 records · Page 7Linked to original sources
PubMed1982

The effect of intraduodenal installation of oleic acid on plasma neurotensin-like immunoreactivity and on gastric acid secretion stimulated by betazole and sham feeding in man.

Intraduodenal administration of oleic acid has previously been shown to inhibit gastric acid secretion induced by pentagastrin in man. This inhibition was dose-dependent and significantly correlated to a rise in plasma concentration of neurotensin-like immunoractivity (NTLI). Maximal inhibition occurred with a volume of oleic acid of 20 ml. In the present study intraduodenal instillation of 20 ml. of oleic acid inhibited acid secretion evoked by sham feeding in healthy subjects but did not significantly inhibit the near-maximal acid secretion stimulated by the histamine analogue betazole. The inhibition of acid secretion induced by sham feeding was the same (about 45%) as the inhibition of pentagastrin-stimulated secretion. Plasma NTLI rose significantly in both the sham feeding and betazole experiments and peaked at about 145 pM. The results are in agreement with the inhibitory characteristics of neurotensin and support the hypothesis that the inhibition of gastric acid secretion by small amounts of intestinal fat is at least partly mediated by neurotensin.

Adult↗
PubMed1982

The effects of secretagogues of isolated human gastric glands.

The function of isolated human gastric glands has been studied in vitro by measuring the 14C-aminopyrine accumulation (RAP) in basal, unstimulated, conditions and after stimulation with different secretagogues. A microscale technique was used which enabled determinations of RAP in tissue obtained as gastroscopic biopsies. In addition, oxyntic-gland-containing mucosa was obtained at gastric resections for gastric or prepyloric ulcer disease. Histamine and cAMP derivative both induced maximal stimulation; RAP was approximately three times larger than in basal states. Carbachol induced a smaller but still significant stimulation. Pentagastrin did not increase RAP above the unstimulated level. Combinations of histamine and carbachol or pentagastrin did not induce a larger response than carbachol alone. The peak acid response to pentagastrin or betazole in vivo did not correlate with the maximum RAP in vitro.

1-Methyl-3-isobutylxanthine↗
PubMed1982

The effect of different anticholinergics on the gastric acid response to sham feeding in man.

Modified sham feeding by the chew and spit technique stimulates gastric acid secretion at a level about 50% of peak acid output. This response is vagal and can be totally blocked by vagotomy. The effect on the acid response to modified sham feeding produced by a quaternary amine, benzilonium bromide, and a presumably more selectively acting antimuscarinic drug, pirenzepine, was compared. The drugs were given 45 min and 10 min before the start of the sham feeding, respectively. Benzilonium bromide, 1 + 1 mg, blocked 73% of the acid response to sham feeding and pirenzepine, 10 + 10 mg, blocked 48% of the response. The difference was not statistically significant. The data confirm that a part, about one third, of the acid response to sham feeding is non-cholinergic, although it is vagal.

Adult↗
PubMed1982

Acid secreting gastric heterotopia in the duodenum.

Heterotopic gastric mucosa was found in the duodenum of a female patient with duodenitis and acid hyposecretion. The heterotopic isolated fundic glands were shown to accumulate 14C-aminopyrine in basal state and on stimulation with histamine suggesting that the heterotopic mucosa secreted acid. The ectopic acid secretion in the duodenal bulb suppressed gastric acid secretion, and might have caused the duodenitis and at least partly the clinical symptoms. The heterotopic gastric mucosa could be removed surgically by local excision. This procedure, combined with a Nissen fundoplication for suspected reflux oesophagitis, was followed by total symptomatic relief and normalization of gastric acid secretion.

Choristoma↗
PubMed1981

Substituted benzimidazoles inhibit gastric acid secretion by blocking (H+ + K+)ATPase.

Studies both in vivo and in vitro have shown that substituted benzimidazoles inhibit the stimulation of acid secretion produced by dibutyryl cyclic AMP and histamine. Furthermore, the results differ from those produced by H2 antagonists and anticholinergic agents in that the inhibition is not competitive, and the site of action is intracellular and peripheral to that of dibutyryl cyclic AMP. To investigate the biochemical mechanism of action of substituted benzimidazoles, one such compound, H 149/94 (2-([2-(3-methyl)pyridyl-methyl]-sulphinyl)-5-methoxycarbonyl-6-methylbenzimidazol), has been tested either directly on an (H+ + K+)ATPase isolated from pig and human gastric mucosa or on the function of this enzyme in gastric glands isolated from rabbit and human gastric mucosa. (H+ + K+)ATPase, which has only been found at the secretory surface of the parietal cell, catalyses a one-to-one exchange of protons and potassium ions. It is possibly the proton pump within the gastric mucosa, and may thus be the terminal or one of the terminal steps of the acid secretory process. We show here that H 149/94 inhibits (H+ + K+)ATPase, which may explain its inhibitory action on acid secretion in vitro and in vivo. Because of the unique distribution and properties of the (H+ + K+)ATPase, the inhibitory action of H 149/94 on this enzyme may be a highly selective clinical means of suppressing the acid secretory process.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1981

A study of the effect of antral distension on gastric acid secretion in man.

In 30 healthy subjects distension of the antrum by a 150-cm3 balloon reduced the acid and volume responses to submaximal stimulation achieved by a continuous intravenous infusion of pentagastrin. The inhibition persisted during perfusion of the stomach with alkaline buffer. The plasma somatostatin concentration did not increase during distension and no somatostatin was detected in the gastric contents. Balloon distension of the antrum during laparotomy did not affect the concentration of somatostatin and gastrin in portal blood in patients with gallbladder disease or duodenal ulcer. The results confirm that antral distension stimulates acid secretion in duodenal ulcer patients without involvement of the gastrin mechanism. Moreover, the inhibition of acid secretion by antral distension in healthy subjects is independent of luminal pH and does not appear to be mediated by somatostatin.

Adult↗
PubMed1981

Fat inhibition of gastric acid secretion in man and plasma concentrations of neurotensin-like immunoreactivity.

The effects of intraduodenal administration of oleic acid (5, 10, 20, and 40 ml) on gastric acid secretion stimulated by a submaximal intravenous pentagastrin infusion and on plasma concentrations on neurotensin-like plasma immunoreactivity (NTLI) were studied in 18 healthy subjects. Each volume of oleic acid or saline (controls) was tested in six subjects except the volume of 20 ml, which was given to ten subjects. Gastric acid secretion was studied for a 2-h period at 15-min intervals after intraduodenal infusion. Five milliliters oleic acid evoked a significant inhibition (29%) of gastric acid secretion. Maximal inhibition by oleic acid appeared after 20 ml (43%), which was significantly greater than after 10 ml. In seven duodenal ulcer (DU) patients 20 ml oleic acid evoked an inhibition of 20%, which was significantly lower than in the healthy subjects. Proximal gastric vagotomy (PGV) abolished the fat inhibition in DU patients. Basal and peak NTLI concentrations after 20 ml oleic acid were significantly lower in DU patients than in health subjects. In DU patients there was no significant difference in the integrated response of NTLI before and after PGV. The 2-h integrated NTLI response was dependent on the administered volume of oleic acid in healthy subjects. There was a correlation between acid inhibition and the integrated response ot NTLI in healthy subjects. This suggests that immunoreactive neurotensin may be involved in the oleic-acid-induced inhibition of gastric acid secretion. Neurotensin, or a neurotensin metabolite, apparently exerts its inhibitory effect at a synaptic level, which explains the finding that oleic acid did not inhibit gastric acid secretion after PGV. Neurotensin may have a physiological role as a hormone with enterogastrone functions.

Adult↗
PubMed1981

Inhibition of pentagastrin-stimulated gastric acid secretion by graded intraduodenal administration of oleic acid in man.

The inhibitory effect of intraduodenally administered oleic acid in volumes of 5--40 ml on pentagastrin-stimulated gastric acid secretion was determined in healthy volunteers. In the control experiments, corresponding volumes of saline were given. Five and 10 ml oleic acid brought about a significant inhibition of gastric acid secretion of 29% and 32%, respectively. After 20 ml of oleic acid the inhibition was 46%, a significantly stronger inhibition than after 5 or 10 ml. Forty milliliters of oleic acid did not further increase the inhibition. Maximal inhibition appeared 30--60 min after the administration of oleic acid. In seven duodenal ulcer patients 20 ml oleic acid evoked an inhibition of gastric acid secretion of 20%, which was significantly less than the inhibition produced in healthy subjects after the same volume of oleic acid. The results suggest that the intraduodenal administration of relatively small volumes of oleic acid elicits a dose-dependent inhibition of pentagastrin-stimulated gastric acid secretion in man and that maximal inhibition is obtained by 20 ml of oleic acid. The results also indicate that duodenal ulcer patients may have a defective fat inhibitory mechanism.

Adult↗
PubMed1980

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.

Adult↗
PubMed1980

The effect of antral distension in healthy subjects on betazole-stimulated gastric acid secretion and the plasma concentration of immunoreactive neurotensin.

Antral distension in seven healthy subjects had the same inhibitory effect, approximately 20% inhibition, on gastric acid secretion stimulated by pentagastrin and betazole (Histalog). The plasma concentration of neurotensin in peripheral venous blood was unchanged during antral distension in healthy subjects. The plasma concentration of neurotensin in portal blood was also unchanged during antral distension in anaesthetized duodenal ulcer patients and in non-ulcer patients. The inhibition of pentagastrin-stimulated gastric acid secretion by balloon distension of the antrum was unchanged by preceding intramuscular injection of metoclopramide. The inhibitory effect of antral distension on gastric acid secretion in healthy subjects does not seem to be mediated by secretin, cholecystokinin, bulbogastrone, neurotensin, or a dopaminergic mechanism.

Adult↗
PubMed1980

The effect of antral distension on the endocrine pancreas in man.

Isolated antral distension by a 150 cm3 balloon in man significantly elevated the plasma concentrations of pancreatic polypeptide and glucagon in portal venous blood. The concentrations of plasma pancreatic glucagon, plasma insulin, and plasma glucose were unchanged in peripheral venous blood during antral distension with or without a background infusion of pentagastrin. Antral distension significantly increased the plasma concentration of pancreatic polypeptide in peripheral venous blood. Antral distension also inhibited basal and pentagastrin-stimulated gastric acid secretion in healthy subjects. The release of pancreatic hormones evoked by antral distension cannot explain the concomitant inhibition of gastric acid secretion. The results support and extend the concept of a gastro-pancreatic reflex to the endocrine part of the pancreas with release of at least pancreatic polypeptide and glucagon.

Adult↗
PubMed1980

The effects of beta-adrenergic receptor blockade on the inhibition of gastric acid secretion, and the release of pancreatic polypeptide by antral distension in healthy subjects.

In a randomized double-blind study of seven healthy subjects an intravenous injection of metoprolol and propranolol did not change the submaximal gastric acid response to pentagastrin. The inhibition of pentagastrin-stimulated acid secretion by balloon distension of the antrum was unchanged by a preceding intravenous injection of metoprolol or propranolol. The plasma level of pancreatic polypeptide in peripheral venous blood showed a significant rise during antral distension. This rise was unaltered by a preceding injection of metoprolol and slightly depressed by propranolol. We conclude that the inhibitory effect of antral distension on gastric acid secretion in healthy subjects is not mediated by beta 1 or beta 2-adrenergic mechanisms. The reflex release of pancreatic polypeptide by antral distension may possibly involve a weak beta 2-adrenergic component.

Adrenergic beta-Antagonists↗
PubMed1980

Management of massive gastroduodenal haemorrhage.

A special program for management of massive gastrointestinal bleeding was 1976 introduced in the surgical service of Sahlgren's Hospital in Göteborg. The main points in this program were: careful observation in an intensive care unit, standardized treatment, early diagnostic gastroduodenoscopy, strict indications for emergency operation and recommendation of type operation. This paper deals with 55 patients subjected to emergency operations in 1976 with the diagnosis erosive gastritis, gastric ulcer or duodenal ulcer. The results are compared to an earlier study in 1962-71 in the same hospital. It was found that the mortality was unchanged during the two periods, 25% during 1962-71 and 24% during 1976. At a first glance the new program might seem ineffective. However, the part of elderly patients was much higher during 1976 than during 1962-71. Thus, the patients during 1976 must be considered much more of a surgical challenge. As old patients often have coexisting severe diseases they are surgically most unfit. Probably a more conservative attitude is justified in this particular group of patients.

Adult↗
PubMed1979

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

Plasma gastrin concentrations and gastric acid output after modified sham feeding were determined in 20 duodenal ulcer patients. Sham feeding produced an acid response corresponding to 40-68% of the maximal acid output after pentagastrin stimulation, with no significant increase of plasma gastrin concentrations. In eight patients proximal gastric vagotomy almost abolished the acid responses to both insulin hypoglycaemia and sham feeding. Sham feeding in the vagotomised patients did not change the gastrin concentrations in plasma. After pretreatment with benzilonium, an anticholinergic with minimal central nervous effects, plasma gastrin concentrations increased after sham feeding. The study confirms that sham feeding is a poor stimulus for gastrin release in duodenal ulcer patients and supports a cholinergic inhibition of gastrin release. Intravenous injection of benzilonium bromide in a dose close to 70 micrograms/kg, and atropine in the low dose of 30 micrograms/kg inhibited the acid response to sham feeding by about 65%. Atropine in a dose of 50 micrograms/kg virtually abolished the acid sham feeding response, possibly owing to ganglionic or central nervous blockade. Vagal activation of the acid secretory glands does not seem to involve a purely cholinergic neurotransmission.

Adult↗
PubMed1979

Vagovagal stimulation of pancreatic-polypeptide secretion by graded distention of the gastric fundus and antrum in man.

Previous studies have shown that pancreatic polypeptide (PP) secretion is regulated by efferent, vagal stimulation. In the present study the afferent part of a vagovagal pathway has been investigated in two different ways: (I) Graded fundic distention: in 8 patients with duodenal ulcer ballon distention with 150 ml of the fundus and the body of the stomach increased PP concentrations in plasma from 19 (17--26) to 41 (35--48) pmol/l, median and interquartile range. Distention by 300 and 600 ml did not further increase PP concentrations. After denervation of the fundus by proximal gastric vagotomy, no increase in PP levels was observed during distention with 50 and 300 ml whereas distention by 600 ml was followed by a small increase. (II) Graded antral distention: balloon distention with 50, 100 and 150 ml of the antrum increased plasma PP concentrations in 7 healthy subjects and 14 duodenal ulcer patients. Maximal PP response was achieved by distention with 100 ml, healthy subjects: from 14 (12--23) to 40 (26--44) pmol/l, and duodenal ulcer patients: from 25 (13--38) to 47 (22--63) pmol/l, median and interquartile range. It is concluded that a gastropancreatic reflex stimulating PP secretion through a long vagovagal pathway is present in man, and that this mechanism probably is involved in the initial PP response during a meal.

Adult↗
PubMed1979

Plasma gastrin concentrations following sham feeding in duodenal ulcer patients.

Sham feeding experiments were performed in 20 duodenal ulcer (DU) patients by using adequate sham feeding and modified sham feeding (the 'chew-and-spit' technique). A 15-min sham feeding induced a marked secretion of gastric acid but only an insignificant increase in total gastrin or in gastrin17 concentrations in plasma. Nor did prolonged sham feeding (30 min) with intragastric neutralization significantly increase the gastrin concentrations. We conclude that sham feeding in DU patients induces a release of recognized gastrin components in amounts that are barely detectable radioimmunologically. Therefore, the acid secretory effects of vagally released gastrins in DU patients remains to be established.

Adult↗