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Biomedical subjects

M C Woussen-Colle

Publications and source records attributed to M C Woussen-Colle.

At least 37 records · Page 2Linked to original sources
PubMed1985

Effects of sham feeding, bethanechol, and bombesin on somatostatin release in dogs.

In seven conscious dogs with esophagostomies and gastric cannulas, the acid, gastrin, and somatostatinlike immunoreactivity (SLI) responses to 5-min sham feeding with or without pretreatment with atropine sulfate (20 and 100 micrograms/kg) were measured. The responses to bethanechol (100 micrograms X kg-1 X h-1), to bombesin (0.5 micrograms X kg-1 X h-1) with or without pretreatment with atropine sulfate, and to a combined stimulation with bethanechol and bombesin were also measured. Sham feeding resulted in an increase in plasma SLI concentration (basal level, 20.4 +/- 4.2 pg/ml; maximally stimulated level, 46.8 +/- 5.6 pg/ml; P less than 0.01). After the injection of atropine the integrated SLI response to sham feeding was significantly decreased but not suppressed. Infusion of bethanechol did not alter SLI plasma levels. Bombesin infused alone increased the plasma SLI concentration (basal level, 15.6 +/- 2.3 pg/ml; maximally stimulated level, 55.6 +/- 10.3 pg/ml; P less than 0.01). The integrated SLI response to bombesin was significantly decreased by atropine but not significantly changed by bethanechol. These studies show that sham feeding and bombesin release somatostatin. They suggest that somatostatin release is largely under vagal-cholinergic control.

Animals↗
PubMed1985

Multiple effects of leucine on glucagon, insulin, and somatostatin secretion from the perfused rat pancreas.

The effects of increasing concentrations of leucine (0.2, 2.0, and 15.0 mmol/liter) on glucagon secretion from the perfused rat pancreas were examined at various glucose levels (0, 3.3, or 8.3 mmol/liter) and in the absence or presence of either arginine (5.0 mmol/liter) or glutamine (10.0 mmol/liter). At a low glucose concentration (3.3 mmol/liter), leucine caused a dose-related biphasic increase in glucagon output in the absence of arginine, but only a transient increase in the presence of the latter amino acid. These positive responses were markedly reduced and, on occasion, abolished at a high glucose concentration (8.3 mmol/liter). Moreover, at a low glucose concentration (3.3 mmol/liter) and in the presence of arginine, the highest concentration of leucine (15.0 mmol/liter) provoked a sustained and reversible inhibition of glucagon release. Likewise, leucine (15.0 mmol/liter) reversibly inhibited glucagon secretion evoked by glutamine in the absence of glucose. Thus, leucine exerted a dual effect on the secretion of glucagon, the inhibitory effect of leucine prevailing at a high concentration of the branched chain amino acid and when glucagon secretion was already stimulated by arginine or glutamine. At a physiological concentration (0.2 mmol/liter), however, leucine was a positive stimulus for glucagon release, especially in the absence of another amino acid. Concomitantly, leucine was always a positive stimulus for both insulin and somatostatin secretion. The intimate mechanisms involved in the dual effect of leucine on glucagon secretion remain to be elucidated.

Animals↗
PubMed1984

Roles of gastrin release and neural reflexes during the gastric phase of acid secretion in dogs.

The acid secretion from the main stomachs and from denervated Heidenhain pouches in response to peptone meals infused in the stomach was determined in 4 dogs. When expressed as percent of the maximal acid response to histamine, the acid secretion from the innervated and from the denervated fundic mucosa was similar, but the response from the Heidenhain pouch was larger when expressed as percent of the maximal response to pentagastrin. These studies indicate that, under the conditions used, short (gastrogastric) and long (vagovagal) reflexes during the gastric phase, are of minor importance in inducing the acid response to the meal.

Animals↗
PubMed1984

Effects of morphine, enkephalins and naloxone on postprandial gastric acid secretion, gastric emptying and gastrin release in dogs.

The effects of intravenous infusions of morphine, met-enkephalin and leu-enkephalin on gastric acid secretion, gastrin release and gastric emptying were investigated in four dogs with gastric cannulas stimulated by a liquid peptone meal. The actions of a potent opiate antagonist, naloxone, used alone or combined with opiates were also studied. Morphine, met-and leu-enkephalin decreased the fractional gastric emptying rate. Acid secretion was decreased by enkephalins and increased by high doses of morphine. Enkephalins and to a lesser degree morphine inhibited gastrin release during the first hour following the administration of the meal. Only leu-enkephalin decreases significantly the integrated gastrin response. Naloxone at the doses used antagonized partly or totally the effects of opiates on gastric emptying but not those on gastric secretion or gastrin release. Naloxone infused alone had no significant effect on the gastric functions tested. These studies indicate that in dogs stimulated by a liquid test meal, enkephalins inhibit gastric emptying, acid secretion and gastrin release. Morphine inhibits gastric emptying and gastrin release and enhances acid secretion.

Animals↗
PubMed1984

[Interactions between secretin and somatostatin on acid secretion and gastric emptying in dogs].

Secretin and somatostatin are two peptides released by H+ ions. The fact that blood levels of these peptides increase during the postprandial period makes them the most probable candidates for gastric acid secretion retrocontrol . The aim of our study was to determine whether a potentiation of inhibitory effects exists when the two peptides are administered simultaneously. Seven dogs were provided with a gastric fistula. Gastric acid secretion was stimulated by intragastric infusion of a bactopeptone solution or by pentagastrin (1 microgram X kg-1 X h-1). Acid outputs and gastric emptying rates were measured at regular intervals. The tests were repeated during intravenous infusion of secretin (0.125 micrograms X kg-1 X h-1), somatostatin (0.2 micrograms X kg-1 X h-1) or both peptides together at the same doses. Both secretin and somatostatin inhibited acid secretion and gastric emptying. The inhibition was not greater when both peptides were administered together. Under the conditions used, no potentiation or additive effects between the two peptides were observed on gastric acid secretion or gastric emptying.

Animals↗
PubMed1984

[Basal concentrations and postprandial integrated flows of gastrin in patients with atrophic gastritis or duodenal ulcer. Limits of diagnostic usefulness].

Maximal acid outputs were determined during intravenous pentagastrin tests (6 micrograms/kg/h) in 119 male subjects: 17 controls, 74 patients with duodenal ulcer and 28 with atrophic gastritis. Basal and postprandial serum gastrin levels were also determined in order to estimate the integrated gastrin response to the meal. In patients with atrophic gastritis the maximal acid output was decreased (p less than 0.01) and the integrated gastric response was increased (p less than 0.01) but the basal gastrin levels in these patients did not differ from that of controls. An integrated gastrin response greater than 2.5 ng/ml/100 min was observed in 89 p. 100 of patients with atrophic gastritis. An integrated gastrin response smaller than 2.5 ng/ml/100 min was observed in 76 p. 100 of controls. The maximal acid output was smaller than 20 mmol/l in all patients with atrophic gastritis but was greater than this value in all controls. In duodenal ulcer patients, the measured parameters were not significantly different from control values. The measure of the integrated gastrin response which reflects the presence of an antral endocrine hyperactivity may be useful to detect patients with atrophic gastritis, but this test is less sensitive and less specific than the determination of the maximal acid output.

Duodenal Ulcer↗
PubMed1984

Effect of met-enkephalin on acid secretion from gastric fistulas and Heidenhain pouches in dogs stimulated by pentagastrin, pentagastrin plus bethanechol, or a meal.

In dogs with denervated Heidenhain pouches and gastric cannulas the authors studied the action of met-enkephalin on acid secretion stimulated by a liquid meal, pentagastrin or pentagastrin + bethanechol. Serum gastrin levels were determined during the feeding experiments. Meal-stimulated and pentagastrin-stimulated acid secretion from the gastric fistula were inhibited by met-enkephalin. A rise in pentagastrin-induced acid secretion was observed in the denervated stomach. No significant changes were observed in the postprandial acid response from the pouch to the meal, nor from the main stomach or the pouch during stimulation with pentagastrin + bethanechol. Gastrin release was decreased by met-enkephalin during the first hour following feeding and increased during the second hour. Our data indicate that met-enkephalin can either inhibit or stimulate acid secretion in dogs. The inhibition occurs only in the innervated fundic mucosa, and might be explained by a decrease in gastrin release and by a decrease in vagal tone.

Animals↗
PubMed1983

[The role of secretin in the control of gastric secretion and emptying in the dog].

It is well established that duodenal acidification strongly inhibits gastric acid secretion, gastric emptying rate and gastrin release. These effects are at least partly mediated via hormonal pathways, but it is not known whether they are mediated by the release of one peptide named in the past enterogastrone, or by several peptides acting together. The effects of duodenal acidification on gastric acid secretion and gastrin release can be reproduced by infusion of small doses of secretin and plasma secretin levels increase during duodenal acidification or after a meal. This peptide is thus the most probable candidate as an enterogastrone. It has however never been clearly shown that administration of low doses of secretin do decrease gastric emptying rate as well as acid secretion. Experiments were performed on four dogs with gastric fistulas. A peptone solution was infused into the stomach. The experiments were repeated during infusion of synthetic secretin. Our results indicate that infusion of low doses of secretin reproduce all the effects of duodenal acidification: a significant inhibition of gastric acid secretion, gastrin release and gastric emptying rate.

Animals↗
PubMed1983

Increase in gastrin and somatostatin cell numbers in the antrum of dogs after small bowel resection.

A proximal 50 p. 100 resection of the small bowel was performed in six dogs while six control animals underwent a simple intestinal transsection and reanastomosis. The pre- and postoperative serum gastrin levels were measured in both groups before and after a standard test meal. The stomach was resected in both groups 6 to 8 weeks after the operation. A morphometric method using specific antigastrin and antisomatostatin antibodies was used to estimate the density and the total number of antral gastrin and somatostatin cells. No variation in basal serum gastrin was found after surgery. A 50 p. 100, though not significant, increase in the postprandial gastrin response was observed after intestinal resection whereas a significant (P less than 0.01) 50 p. 100 increase in the gastrin cell density was found in the antral mucosa of these dogs. At the same time, a remarkable hyperplasia of the antral somatostatin cell population was observed in the animals submitted to small bowel resection.

Animals↗
PubMed1980

Antral gastrin cell hyperplasia in patients with peptic ulcer.

The total number of gastrin (G) cells in the stomach was determined by using a histologic counting method and planimetry in ulcerous and nonulcerous patients. The preoperative basal and postprandial serum gastrin values and the gastrin cell mass in the gastrectomy specimen could be compared in 16 surgical patients. There was a significant correlation between the integrated gastrin response to feeding and the total gastrin cell number in the stomach. No correlation was found between the basal serum gastrin level and the total gastrin cell count. A total gastrin cell number higher than 50 million was found in the stomach of three duodenal ulcer patients with preoperative postprandial hypergastrinemia as well as in one patient with normal serum gastrin values. Gastrin cell counts between 6 and 42 million were found in control stomachs and in patients with gastric ulcer. Preoperative feeding tests could be useful to select patients with an elevated antral G cell number.

Cell Count↗
PubMed1978

Estimation of the antral and duodenal gastrin cell population removed by gastrectomy from patients with peptic ulcer.

The total number of gastric and duodenal gastrin cells was determined in the gastrectomy specimens from eight patients with peptic ulcer. Planimetry was used to determine the antral and duodenal surface. The immunoperoxydase method with specific antigastrin antibodies was used for staining gastrin cells, and the mean concentration of nucleated gastrin cells per square millimeter of antral and duodenal surface was determined by light microscopy. The mean number of duodenal gastrin cells in the resected duodenum was 4.8 per cent of the total gastric gastrin cell mass. The concentration of gastrin cells in the antrum was quite variable from one mucosal site to another. The degree of extension of the antral gastritic areas was a major factor influencing the mean concentration value. The total number of gastrin cells in the stomach varied from approximately 7 to 74 million cells. Our data indicate that hyperplasia of gastrin cells cannot be demonstrated by studies performed in small specimens taken for biopsy.

Cell Count↗
PubMed1977

Relationship between disposal rate of exogenous gastrin and sensitivity to stimulation of acid secretion by this hormone in dogs.

The effect of graded doses of synthetic human gastrin and pentagastrin on gastric secretion from the innervated and denervated stomach was measured in dogs. The circulating levels of gastrin during the infusion of this hormone were also estimated. The increase in gastrinemia for a fixed dose of exogenous gastrin differed from dog to dog. The dose for half-maximal response to gastrin was negatively correlated with the observed increase in serum gastrin. This suggests that the disposal rate of gastrin influences the calculated sensitivity of the parietal cells to this hormone. In the gastric fistula and in the pouch, maximal acid responses for gastrin and pentagastrin were linearly correlated, but doses for half maximal responses were not. This indicates that step-dose infusion of pentagastrin may be used to estimate the maximal acid response to gastrin, but it is not proven that such a test is useful to estimate the sensitivity of the parietal cells to gastrin in individual dogs.

Animals↗
PubMed1977

Relationship of the gastrin response to the amount of food ingested in normal subjects.

The serum gastrin response to three different amounts of a same meal was studied in 8 normal subjects. The peak gastrin response was similar for the three meals, but the integarated gastrin response was larger with the largest meals. Comparison of the response to the two largest meals indicates that in a given subject the gastrin response is similar when test on different occasions. A good correlation was found between individual fasting concentrations of gastrin and peak gastrin levels after feeding but not between basal gastrin and integrated gastrin response. This could indicate that in normal subjects the first two parameters are primarily related to the same control mechanisms (possibly the G cell mass), while the integrated gastrin response reflects the effectiveness of the feedback mechanisms controlling gastrin release.

Food↗