Search PubMed⌕ Search

Biomedical subjects

F Stadil

Publications and source records attributed to F Stadil.

At least 109 records · Page 6Linked to original sources
PubMed1975

Effect of histamine on immunoreactive gastrin in gastric juice and in serum.

Due to recent reports claiming that gastrin is present in the gastric juice, the method for gastrin determination has been evaluated. Separate experiments showed that gastrin added to gastric juice disappears rapidly if the juice is not boiled or neutralized. A total of 82 patients with various abdominal disorders were examined. No or only a trace amount of gastrin was found in untreated, boiled, or boiled and neutralized gastric juice in every patient, including three patients with achlorhydria. Histamine injection (0.04 mg. per kilogram, subcutaneously) did not influence this and was without effect upon serum gastrin concentrations of nine duodenal ulcer patients. Because gastrin apparently is degraded rapidly by gastric juice, this study does not necessarily disprove that gastrin is secreted into the stomach. However, the virtual absence of gastrin in all specimens examined, including some collected directly upon boiling water bath during continuous gastric aspiration lends no support to this speculation. Because gastrin does not survive even a short exposure to gastric juice without degradation, we suggest that earlier reports on the presence of gastrin within the stomach are questionable.

Achlorhydria↗
PubMed1975

Measurement of immunoreactive gastrin in gastric mucosa.

A method for measurement of gastrin in gastric mucosa has been developed, and distribution of gastrin in the stomach of pig, dog, cat, rabbit, and man was examined. Measurable amounts of gastrin were found in corpus of all species, but the content in the antrum was considerably higher. The highest concentration of gastrin was seen in man. The borderline between corpus and antrum was abrupt, and in both parts of the stomach gastrin was evenly distributed. In 44 patients with duodenal ulcer the antral gastrin concentration was 21.3 mug eqv. per g mucosa, in 15 patients with prepyloric ulcer 23.0, in 10 patients with gastric ulcer 5.9, and in 16 patients with gastric carcinoma 7.9. The control group consisted of 10 healthy volunteers and 12 patients with minor abdominal complaints. Mean antral gastrin concentrations were 28.1 and 20.7 respectively. No significant relationship was observed between PAO and gastrin content of antral mucosa in any group.

Adult↗
PubMed1975

Beta-adrenergic mechanisms and ulcer formation in pylorus-ligated rats.

The importance of beta-adrenergic receptor activity for ulcer formation was studied. In rats fasted for 48 hours, ulcers in the rumen were produced constantly after 17 hours of pyloric ligation. d,1,Propranolol in doses of 1 to 30 mg/kg given 4 times during 12 hours caused a dose-dependent inhibition of ulcer formation. The ulcero-protective potency of d,1,propranolol was about 20 times that of d,propranolol. No explanation of the ulcero-protective effect was observed when the gastric acid secretion was studied after 17 hours. Serum gastrin concentration after 17 hours of ligation was in all animals less than 5 pmol per liter, i.e. below one-third of the normal fasting value. For all pharmacological effects apart from beta-adrenergic blockage, d,1, and d,propranolol do not differ, while the results presented here suggest that intact beta-adrenergic receptor activity is important for the development of gastric ulcers in the pylorus-ligated rat. The mechanism behind the ulcero-protective effect of beta-adrenergic blockage remains to be solved.

Animals↗
PubMed1975

Patterns of gastrin components in serum during feeding in normal subjects and duodenal ulcer patients.

The contribution of the different gastrin components to the gastrin response to a protein-rich meal was studied. Pooled or individual samples of venous blood drawn at intervals in 12 normal subjects and 16 patients with duodenal ulcers were fractionated on Sephadex G 50 superfine columns of various lengths. Total gastrin immunoreactivity and concentrations of various components were measured radioimmunochemically. The changes in total serum concentration of immunoreactive gastrin were principally due to changes in component II ('big gastrin') and III ('little gastrin'). The predominant pattern in both groups was an early increase in component III and a later and smaller increase in component II. Total gastrin response was largest in the patients with duodenal ulcer, and this was due mainly to component III. Furthermore, fasting samples also showed a relatively higher concentration of component III in the ulcer patients. This study shows that 'little gastrin' is the more important component in the gastrin response to stimulation by food. Serum concentrations of total gastrin immunoreactivity are alike in normal subject and duodenal ulcer patients, but the findings indicate that increased levels of 'little' gastrin may be characteristic of duodenal ulcer disease. Since 'little gastrin' is more potent than 'big gastrin', this would agree with the hypersecretion of acid in duodenal ulcer.

Duodenal Ulcer↗
PubMed1975

Mixed endocrine pancreatic tumors producing several peptide hormones.

Twenty-four endocrine pancreatic tumors were examined immunohistochemically for insulin, glucagon, gastrin and ACTH. In seven of these tumors, more than one peptide-hormone-containing cell type was observed. These seven tumors were also examined with conventional staining methods for the presence of A1, A2, and B cells. The results showed that these staining methods do not always distinguish between the different hormone-producing cell types of endocrine pancreatic tumors. In spite of the fact that several types of hormone-secreting cells were found in the tumors, the case histories described symptoms characteristic of hypersecretion of only one of the hormones. The hormone of the predominating cell type could not always explain the clinical symptoms. Our results indicate the endocrine pancreatic tumors often are multihormonal. Therefore, it would seem advisable to screen serum from all insuloma patients for a variety of peptide hormones.

Adrenocorticotropic Hormone↗
PubMed1975

Interaction of calcium and magnesium on gastric acid secretion and serum gastrin concentration in man.

The effect of magnesium on calcium- and pentagastrin-induced gastric acid secretion and on calcium-induced gastrin secretion were studied in healthy volunteers. Intravenous infusion of calcium gluconate increased serum gastrin concentration as well as gastric volume secretion, acidity, and acid output. Addition of magnesium sulfate to the infusion caused a slight but insignificant increase in serum gastrin concentration, whereas volume secretion, acidity, and acid output were significantly depressed. Intravenous infusion of magnesium sulfate had no effect on gastric acid secretion induced by a submaximal pentagastrin infusion. The results indicate that magnesium antagonizes the activation of gastric acid secretion by calcium without suppressing gastrin release and may suggest that magnesium does not change the sensitivity of the parietal cell to gastrin.

Adult↗
PubMed1974

Correlation between serum gastrin concentration and rat stomach histidine decarboxylase activity.

After prolonged fasting the activity of histidine decarboxylase in the oxyntic mucosa of the rat stomach is low. Feeding or injection of gastrin or insulin rapidly raises the enzyme activity. It was earlier suggested that all enzyme-activating agents act through release of gastrin. This view has found experimental support in studies which show that in antrectomized rats the enzyme is activated by gastrin but not by gastrin-releasing stimuli like feeding or vagal excitation (insulin hypoglycemia). In the present investigation rats were subjected to a variety of treatments and serum gastrin concentrations and gastric histidine decarboxylase activities were measured. The main findings were as follows.1. Feeding raised the serum gastrin level and the enzyme activity in unoperated rats. In fasted antrectomized rats the serum gastrin concentration was low; in freely fed antrectomized rats it was at the same level as in fasted unoperated rats. In antrectomized rats the enzyme activity was low and not raised by feeding.2. Acid in the antrum inhibits the release of gastrin whereas an alkaline pH may facilitate such release. All treatments that blocked acid secretion, thereby raising the antral pH, also raised the serum gastrin concentration and concomitantly the histidine decarboxylase activity. Thus, vagotomy increased the serum gastrin level and the histidine decarboxylase activity in fasted rats. Treatment of fasted unoperated rats with atropine or hexamethonium had similar effects. Antral exclusion, which prevents HCl from reaching the pyloric glands, resulted in marked increase in the serum gastrin concentration and in the enzyme activity of fasted rats.3. Injection of insulin resulted in a rather slow, progressive increase in the serum gastrin concentration. The peak was reached after about 4 hr. The enzyme activity was also raised markedly and the peak response occurred about 1 hr later.4. An increase in the histidine decarboxylase activity was invariably preceded or accompanied by a raised serum gastrin level. With fasted or fed unoperated, vagotomized, antrectomized or antrally excluded rats, the correlation coefficient for the relation between enzyme activity and serum gastrin concentration was 0.69 (P < 0.05).5. Porta-caval-shunted fasted rats responded to feeding or injection of insulin with marked activation of gastric histidine decarboxylase. The response after feeding was at least 5 times higher in shunted than in nonshunted rats but serum gastrin was only slightly higher. Following antrectomy of porta-caval-shunted rats feeding no longer raised the enzyme activity. Thus, the enzyme-activating agent was of antral origin. In the shunted rats injection of pentagastrin induced an enzyme activation about 5 times that seen in intact rats. This response was not significantly reduced by antrectomy. In conclusion, we have observed a correlation between serum gastrin concentration and histidine decarboxylase activity. We have failed to obtain evidence for the existence of any physiological intermediate other than gastrin in the activation of histidine decarboxylase induced by feeding, vagal stimulation or inhibition of acid secretion.

Animals↗
PubMed1974

Immunoreactive gastrin components in human serum.

The apparent molecular size and charge of immunoreactive gastrin components were studied in sera from patients with pernicious anaemia or gastrinomas (the Zollinger-Ellison syndrome) by Sephadex gel filtration and aminoethylcellulose chromatography. The following serum components were distinguished: (1) a monophasic component I similar in size to proinsulin which was converted into ;little' gastrin I by trypsin digestion; (2) a biphasic component II, corresponding to ;big' gastrins I and II (Gregory and Tracy); (3) a biphasic component III corresponding to ;little' gastrins I and II (Gregory and Tracy); and (4) a biphasic component IV, corresponding to ;minigastrins' I and II (Gregory and Tracy). ;Big, big' gastrin, a plasma component found in the void volume of the Sephadex G-50 column by Yalow and Berson (1972) was undetectable in the sera investigated. A component in gastrinoma and antral mucosa extracts corresponding in size to ;big big' gastrin was detectable by the assay; the ;big big' gastrin fraction from gastrinoma tissue was heterogenous, with components of apparent MW 30 000-100 000. It is concluded that serum gastrin circulates in the form of at least four components, of which the three smaller ones are in pairs.

Anemia, Pernicious↗
PubMed1974

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.

Adult↗
PubMed1974

Effect of atropine on gastrin and gastric acid response to peptone meal.

The action of intravenous atropine on meal-and pentagastrin-induced gastric acid secretion was studied in six duodenal ulcer patients.A test meal of 10% peptone solution adjusted to pH 5.0 was maintained in the stomach at at distention presure of 15 cm H(2)O, and a modification of the intragastric titration method of Fordtran and Walsh was used to measure gastric acid output by monitoring the rate at which a solution of 0.5 M sodium bicarbonate had to be added to keep the pH of the gastric content constant at the initial (pH 5.0) value. Serum gastrin concentrations were measured simultaneously by radioimmunoassy. The dose of 25 mug/kg-h atropine inhibited meal-induced acid secretion by about 70% and that evoked by pentagastrin by about 30%. The serum gastrin response to the test meal was not significantly altered by atropine. We conclude that atropine is a very strong inhibitor of meal-induced gastric acid secretion and does not significantly change serum gastrin response to feeding in duodenal ulcer patients when postprandial gastric acidity (pH 5.0) and intragastric pressure (15 cm H(2)O) are kept constant.

Adult↗