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Biomedical subjects

A K Sandvik

Publications and source records attributed to A K Sandvik.

At least 91 records · Page 5Linked to original sources
PubMed1991

Pentagastrin-stimulated histamine release and acid secretion from the totally isolated vascularly perfused rat stomach.

This study was performed to examine the effect of cAMP levels on histamine release in the isolated rat stomach. Pentagastrin-induced histamine release was unaffected by phosphodiesterase inhibition, and pentagastrin itself had no phosphodiesterase-like effect. The results support previous observations showing that histamine is likely to be the mediator of the acid secretagogue effect of (penta) gastrin.

1-Methyl-3-isobutylxanthine↗
PubMed1991

CCK-B (gastrin) receptor regulates gastric histamine release and acid secretion.

To study the interdependence between gastric histamine release and acid secretion, we examined the effects of gastrin-(1-17) [G-(1-17)] or cholecystokinin-(1-33) [CCK-(1-33)] alone or combined with the gastrin (CCK-B) antagonist L365,260 or the CCK-A antagonist L364,718 in the isolated vascularly perfused rat stomach. G-(1-17) and CCK-(1-33) gave concentration-dependent increases in acid secretion and histamine release. Gastrin or CCK-A antagonist alone did not stimulate histamine release or acid secretion. Maximally G-(1-17) or CCK-(1-33) stimulated histamine release and acid secretion was unchanged by the CCK-A antagonist, while the gastrin antagonist induced a parallel and concentration-dependent decrease in stimulated histamine and acid secretion. We conclude that G-(1-17) and CCK-(1-33) stimulate histamine and acid secretion by a CCK-B (gastrin) receptor. The present results indicate that gastrin, at least in this species, stimulates acid secretion by releasing histamine.

1-Methyl-3-isobutylxanthine↗
PubMed1991

Relationship between endoscopic hiatus hernia and gastroesophageal reflux symptoms.

Little is known about the relationship between hiatus hernia (HH) and gastroesophageal reflux symptoms (GERS). Nine hundred and thirty patients submitted to gastroscopy because of symptoms completed a self-administered questionnaire. Fourteen per cent showed esophagitis (ES) and 17% HH. Forty-nine per cent of the patients with HH had endoscopic ES, and 60% of those with ES had HH. The severity of ES was dependent (p less than 0.05) on both the presence and the size of HH. After exclusion of patients with peptic ulcer and malignancy, patients with and without HH and ES were compared with regard to the presence of single symptoms and a weighted GERS score based on symptoms proven to be typical for ES. Only borderline differences were found between patients with ES and HH and those with ES and no HH. The former group, however, presented with significantly (p less than 0.001) more GERS than the patients with HH only. Nevertheless, the patients with HH as the only pathologic finding had significantly (p less than 0.01) more GERS than the patients with no major endoscopic abnormality. This study indicates a close association between HH and gastroesophageal reflux disease and supports the clinical significance of an endoscopically detected HH.

Adult↗
PubMed1991

Effect of the histamine-1 antagonist astemizole alone or with omeprazole on rat gastric mucosa.

The stimulation of acid secretion by gastrin may in the rat be explained solely by gastrin-induced histamine release. This study was done to examine whether histamine could mediate the general trophic effect of gastrin on the oxyntic mucosa, by using a long-acting selective histamine-1 antagonist (astemizole) alone or with omeprazole-induced hypergastrinaemia for 90 days in female Sprague-Dawley rats. At day 90, isolated vascularly perfused rat stomachs were prepared to study maximal gastrin- and histamine-stimulated acid and pepsinogen outputs and maximal gastrin-stimulated histamine release. Oxyntic mucosa morphometry, mucosal histamine and pepsinogen contents, and plasma gastrin and histamine levels were also determined. For the first time, omeprazole has been found to inhibit gastric emptying and to increase plasma histamine. As compared with controls, astemizole alone did not influence plasma gastrin, increased plasma histamine in only some rats, and gave a slight increase in all other variables. Together with omeprazole, it further increased variables already stimulated by omeprazole. Thus, mucosal thickness, histamine concentration, and chief-cell density in oxyntic mucosa were significantly higher in astemizole/omeprazole-treated rats than in omeprazole-treated rats. Gastrin-stimulated histamine release was increased in both astemizole- and omeprazole-treated rats. For all rats plasma histamine was significantly correlated with plasma gastrin and with numerical fundic argyrophil cell density. In conclusion, the present study confirms the trophic effect of gastrin and shows a slight trophic effect of astemizole on the oxyntic mucosa. It also shows that plasma histamine may reflect the argyrophil cell density in the oxyntic mucosa and that omeprazole inhibits gastric emptying.

Animals↗
PubMed1991

The effect of omeprazole-induced hypergastrinemia on the oxyntic mucosa of mastomys.

Mastomys is a rodent with a high incidence of spontaneous carcinoids in the acid-producing part of the stomach. The present study was conducted to examine whether hypergastrinemia could promote tumor formation in this species. Mastomys, 4 months of age, were treated for 5 months with omeprazole subcutaneously, 100 mumol/kg body weight daily, and compared with mastomys given the vehicle only. The plasma gastrin concentration and the number of antral gastrin cells were increased in the omeprazole-treated group. The hypergastrinemia was associated with elevated histidine decarboxylase activity and histamine content in the oxyntic mucosa and with a trophic effect on the oxyntic mucosa and the enterochromaffin-like cells. However, no carcinoid tumors were observed, possibly because the strain of mastomys studied does not produce carcinoids spontaneously.

Animals↗
PubMed1991

Radioimmunoassay of histamine.

Histamine is formed by decarboxylation of the amino acid histidine and is found both in plants and in animals, including man. In man it has important biologic functions. To assess the physiologic role of histamine, however, it is necessary to have a reliable and convenient method to determine its concentration in biologic fluids and tissue. Histamine has been determined by bioassay, chemically by different modification of a fluorometric method, by radioenzymatic methods, and, recently, by immunoassays. Immunoassay of histamine has, however, been difficult to establish, mainly as a result of problems with the production of an antibody with histamine specificity. This is due to the general occurrence of histamine in all animal species. By binding histamine to different ligands, several researchers have succeeded in producing antibodies against antigens in which histamine is integrated. Treating samples and histamine standard with the same coupling agent, reliable and specific radioimmunoassays of histamine have been established. We have for some years utilized a commercial radioimmunoassay of histamine and confirmed its convenience, specificity, and sensitivity. In some patients taking a histamine-2 blocker (cimetidine or ranitidine) we have detected an increase in plasma histamine which also tended to be increased after proximal gastric vagotomy and in patients with gastric ulcer compared with patients with duodenal ulcer. In rats treated with high doses of omeprazole for 90 days we found an increase in the enterochromaffin-like cell mass and in histamine concentration in the oxyntic mucosa which was reflected by an increase in plasma histamine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Aspects of the regulation of gastric histamine release.

Histamine is found in large amounts in the gastric mucosa and plays an essential role in the regulation of acid secretion. It is thought to stimulate acid secretion directly after being released by the other two major secretagogues (gastrin and acetylcholine) (the mediator hypothesis) or to potentiate the action of the other two secretagogues (the interaction hypothesis). Recent studies with isolated, vascularly perfused rat stomach have shown that gastrin in physiologic concentrations elicits a release of histamine sufficient to explain its acid-stimulatory effect. Vagal nerve stimulation, on the other hand, only gives a faint histamine release, indicating that the vagal acid stimulation is mainly mediated by a direct stimulation of the parietal cell. Furthermore, the gastrin-stimulated histamine release seems to be mediated by a calcium-dependent mechanism. Somatostatin inhibits gastrin-stimulated histamine release via a paracrine mechanism, and a prostaglandin E1 analogue (misoprostol) has been shown to be a potent inhibitor of base-line and gastrin-stimulated histamine release. These studies show that the modulation of histamine release may be a central regulatory mechanism of gastric acid secretion. Although these studies have been done in rats, there are indications that these results are of a general nature nd valid for other species as well.

Animals↗
PubMed1991

Trophic effect of histamine on the stomach.

On the basis of clinical observations and experimental animal studies it has been established that gastrin has a trophic effect on the oxyntic mucosa. On the other hand, histamine, being at least as efficient as gastrin as an acid secretagogue, has experimentally been reported not to have such trophic effect. However, during the last few years both endogenously and exogenously induced hypergastremia have been shown to have a specific trophic effect on the enterochromaffin-like (ECL) cell and a less pronounced and later detectable general trophic effect on the oxyntic mucosa. Moreover, in the rat (the species in which most of the trophic studies have been done) the acid-stimulatory effect of gastrin may be solely explained by stimulation of histamine release from ECL cells. Therefore, it seemed natural to evaluate whether the general trophic effect of gastrin could also be caused by histamine or another substance released from the ECL cells. In this review we challenge the concept that maximal pentagastrin-stimulated acid secretion only reflects the parietal cell mass, since the acid-stimulatory effect of gastrin is mediated by histamine release. Therefore, maximal pentagastrin-stimulated acid secretion reflects both the ECL cell mass and the parietal cell mass. With regard to the possible trophic effect of histamine, we show that the doses previously used have been inadequate. Furthermore, histamine has been reported to have a trophic effect on the parietal cell in the dog; some patients with hyperhistaminemia have an increased maximal histamine-stimulated acid secretion, suggesting an increase in the parietal cell mass; and there is parietal cell hyperplasia in the oxyntic mucosa surrounding the histamine-producing carcinoids in mastomys.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Enterochromaffin-like tumour cells in the diffuse but not the intestinal type of gastric carcinomas.

Gastrin may play a role in gastric carcinogenesis, as indicated by an increased frequency of gastric carcinomas in patients with pernicious anaemia and the fact some human gastric cancer cell lines carry the gastrin receptor. Recently, it has been shown that the acid-stimulatory effect of gastrin may be solely mediated by histamine release from the enterochromaffin-like (ECL) cell, on which gastrin has a specific trophic effect. We therefore found it of interest to examine human gastric carcinomas for the presence of ECL tumour cells by using silver staining and chromogranin immunohistochemistry. We found evidence of ECL cell-derived tumour cells in 40% of the diffuse gastric carcinomas but no such tumour cells in the intestinal type of gastric carcinoma. This may suggest that diffuse gastric carcinomas, like malignant gastric tumours of the mastomys, are in fact malignant ECLomas.

Carcinoma↗
PubMed1990

Rat gastric histamine release: a sensitive gastrin bioassay.

Acid secretion and histamine release from the totally isolated vascularly perfused rat stomach are sensitive parameters for the biological effects of gastrin. By optimalizing the Ca2+ concentration of the vascular perfusate the sensitivity for stimulation of acid secretion was improved from 65 to 16 pmol/l gastrin 1-17 (G-17). Measurement of venous histamine before and after gastrin in each stomach preparation excluded inter-stomach variability and improved the sensitivity to 2 pmol/l G-17. This is the most sensitive gastrin bioassay reported, with a detection limit comparable to that of radioimmunoassay.

Animals↗
PubMed1990

The predictive value of history in dyspepsia.

Symptomatic patients referred to an open-access upper gastrointestinal endoscopy completed a detailed, self-administered questionnaire aimed at assessing the predictive value of history in dyspepsia. Nine hundred and thirty patients were suitable for analysis. Of these, 29% were found to have organic dyspepsia. A substantial overlap of symptoms and demographic data was found among the various endoscopic diagnoses. Discriminating variables were identified by stepwise logistic regression analysis and included in predictive score models. Pain relieved by antacids, age above 40 years, previous peptic ulcer disease, male sex, symptoms provoked by berries, and night pain relieved by antacids and food were found to predict organic dyspepsia with a sensitivity and specificity of approximately 70%, when applied on the observed material. Similar probabilities were found for score models of peptic ulcer and esophagitis. In general, the low prevalence of organic diseases resulted in low positive and high negative predictive values. Accordingly, the main impact of the predictive models may be to reduce the number of negative endoscopies rather than to predict a precise diagnosis. Independent of disease category and age, 41% of the subjects expressed a fear of malignancy, emphasizing the value of reassurance from a negative endoscopy.

Adult↗
PubMed1990

The benefit of colonoscopy.

In a prospective study involving 833 consecutive outpatient and open-access colonoscopies, attempts were made to characterize the benefit of colonoscopy in terms of both predicted and unpredicted findings and therapeutic procedures. The endoscopist therefore predicted the endoscopic findings before the endoscopy. The results were compared for the different indications for colonoscopy. The overall agreement between the predictions and the colonoscopic findings was 61%. Clinically significant abnormalities were found in about half the examinations. The most frequent abnormal findings were benign polyps (24%), inflammatory bowel disease (17%), and malignancy (5%). In about half the patients with a malignancy the indication for colonoscopy was rectal bleeding, and half of the malignancies were not predicted. The greatest benefit of colonoscopy was found in patients referred because of overt rectal bleeding or occult faecal blood, and abnormal barium enema or endoscopy findings. The importance of complete colonoscopy in connection with operation for colorectal carcinoma is emphasized.

Colonic Polyps↗
PubMed1989

Histamine release in the isolated vascularly perfused stomach of the rat: regulation by autoreceptors.

1. In the isolated vascularly-perfused stomach of the rat, gastrin 1-17 (520 pmol 1(-1)) increased acid output from basal values of 13.7 +/- 2.7 to 92.5 +/- 11.4 mumol h-1 and venous histamine output from 10.1 +/- 2.3 to 54.7 +/- 7.9 nmol h-1 (mean +/- s.e.mean). 2. The H1 receptor agonist 2-methylhistamine (10 mumol 1(-1)) increased acid output to 21.6 +/- 2.9 mumol h-1 (P less than 0.05) and reduced basal histamine output to 4.0 +/- 0.8 nmol h-1 (P less than 0.05). Gastrin-stimulated acid secretion and vascular histamine output was not significantly affected by 2-methylhistamine (10 mumol 1(-1)). 3. The H2 receptor agonist, impromidine, dose-dependently increased basal acid secretion, reaching a maximal value of 145.5 +/- 11.7 mumol h-1 with impromidine (10 mumol 1(-1)), and maximal gastrin-stimulated acid secretion to 167.4 +/- 15.1 mumol h-1 with impromidine (10 mumol 1(-1)). Impromidine dose-dependently inhibited basal and gastrin-stimulated vascular histamine output. 4. The H3 receptor agonist R-a-methylhistamine, (1 and 10 mumol 1(-1)) minimally increased basal acid secretion. R-a-methylhistamine (10 mumol 1(-1)) did not significantly affect maximal gastrin-stimulated acid secretion. Basal and gastrin-stimulated vascular histamine outputs decreased to 4.0 +/- 0.8 (P less than 0.05) and 24.7 +/- 4.7 nmol h-1 (P = 0.05) with R-a-methylhistamine (10 mumol 1(-1)). 5. The H2 receptor antagonist ranitidine (2 mumol 1(-1)) did not inhibit basal acid secretion, but acid outputs with gastrin and all histamine agonists were reduced. Ranitidine did not affect histamine release in the basal state, with gastrin or with any histamine agonist tested. 6 We conclude that gastric histamine release in the rat is regulated via a histamine H2 receptor sensitive to the histamine agonists tested, but not to ranitidine. It is unlikely that the inhibition of histamine release is secondary to increased gastric acidity.

Animals↗
PubMed1989

Histamine and gastrin in plasma of patients with upper gastrointestinal diseases.

The etiology of peptic ulcer disease is completely unknown. However, gastric acid secretion plays an important role in the pathogenesis of the disease. Acetylcholine, gastrin and histamine are recognized as the main stimulators of the acid secretion. Extensive studies on blood gastrin have not incriminated this hormone in the pathogenesis of the disease. The present study was done to evaluate the role of circulating histamine in peptic ulcer disease using a sensitive and specific radioimmunoassay method. Since gastrin at least in some species seems to exert its stimulatory effect by releasing histamine, serum gastrin was also determined. There was no significant difference in plasma histamine between patients with duodenal or gastric ulcer, nonulcer dyspepsia or ulcer patients after proximal gastric vagotomy. However, patients taking a histamine-2 blocker (cimetidine or ranitidine) had significantly higher plasma histamine than those not taking these drugs. This effect was not due to interference in the histamine assay. There was no correlation between plasma histamine and plasma gastrin. Plasma gastrin was significantly increased in patients having been operated on with a proximal gastric vagotomy. In conclusion, plasma histamine is similar in patients with different upper gastrointestinal disorders. However, histamine-2 blockers may increase plasma histamine.

Blood Specimen Collection↗
PubMed1989

The effect of gastrin-releasing peptide on acid secretion and the release of gastrin, somatostatin, and histamine in the totally isolated, vascularly perfused rat stomach.

We have studied the effect of gastrin-releasing peptide (GRP) on exocrine and endocrine secretion in the totally isolated, vascularly perfused rat stomach with or without concomitant infusion of a potent somatostatin antiserum. GRP (1 nM) showed a marginal acid-stimulatory effect (base line, 11.6 +/- 2.3 mumol/60 min, and after GRP, 20.0 +/- 2.2 mumol/60 min; p = 0.05). GRP significantly increased gastrin and somatostatin release to the venous effluent, and the venous gastrin concentration increased significantly during concomitant infusion of somatostatin antiserum. Furthermore, GRP inhibited histamine liberation, and somatostatin antiserum reversed this effect. The antiserum did not significantly stimulate acid secretion. Thus, the present study shows that GRP directly or indirectly affects both acid secretion and the release of gastrin, somatostatin, and histamine in the rat stomach.

Animals↗