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Biomedical subjects

J De Graef

Publications and source records attributed to J De Graef.

At least 19 recordsLinked to original sources
PubMed1991

Treatment of high-output gastric fistulas with omeprazole.

Two patients with high-output gastrocutaneous fistulas were treated with total parenteral nutrition and gastric antisecretory drugs. IV administration of omeprazole decreased acid output in one patient in a rapid and significant way, resulting in the spontaneous healing of the fistula after eight days of treatment. In the second patient, omeprazole caused a marked reduction in the acidity of the fluid in the fistula, which also closed without surgical operation. The long-standing decrease in acid output induced by intravenous omeprazole may be very useful for promoting spontaneous closure of high-output gastrocutaneous fistula.

Gastric Fistula↗
PubMed1989

Effect of acute suppression of acid secretion by omeprazole on postprandial gastrin release in conscious dogs.

The effect of acute suppression of acid secretion induced by administration of a single dose of omeprazole (2 mg/kg body wt) on postprandial gastrin release was studied in 10 conscious dogs. In omeprazole-treated dogs, a sustained gastrin release was observed during a 10-h period after feeding, although greater than 95% of the meal had left the stomach after 4 h. This sustained gastrin release could be inhibited by acidification of the gastric lumen, by somatostatin, and by atropine. Insulin and bombesin induced considerable gastrin release in omeprazole-treated dogs, but plasma gastrin concentrations returned almost to basal values after 3 h. Omeprazole administered alone had no significant effect on basal gastrin levels. These data indicate that, in dogs, when acid secretion is suppressed by omeprazole a meal induces a sustained gastrin release lasting for up to 10 h. This gastrin release is probably related to the fact that food has been in contact with the gastric lumen, as neither vagal nor bombesin stimulation induced such a sustained activity of the G cells.

Animals↗
PubMed1988

Effect of cimetidine, ranitidine and omeprazole on postprandial gastrin and somatostatin release in conscious dogs.

During a first series of experiments, the gastrin responses to a meal were measured and compared to the responses seen after administration of cimetidine (2.5 mg/kg/h) or omeprazole (2 mg/kg). During a second series of experiments the effects of cimetidine (2.5 mg/kg/h), ranitidine (0.5 mg/kg/h) and omeprazole (2 mg/kg) on post-prandial gastrin and somatostatin release were determined in experiments during which the intragastric pH was maintained close to 6.4. During a third series of experiments, the effects of cimetidine (2.5 mg/kg/h) and omeprazole (2 mg/kg) on basal gastrin and somatostatin release were estimated. Postprandial gastrin release was increased by cimetidine and by omeprazole. When acidification of the gastric content was prevented by intragastric titration, postprandial gastrin release was increased by about 100%. No further increase was observed when the animals were concomitantly treated with cimetidine, ranitidine or omeprazole. Intragastric titration did not alter postprandial somatostatin release. Concomitant administration of H2 blockers decreased the somatostatin response to the meal, while concomitant administration of omeprazole did not alter this release. No significant changes were observed in basal gastrin or somatostatin levels after administration of cimetidine or omeprazole.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Effect of vagotomy and atropine on plasma somatostatin response to a meal in conscious dogs.

In 4 conscious dogs with gastric fistulas the somatostatin responses to a meal were measured and compared to the responses seen after i.v. infusion of atropine sulfate (20 and 50 micrograms.kg-1.h-1) or cimetidine (8 mg.kg-1.h-1). The experiments were repeated after truncal vagotomy. The somatostatin responses to bombesin (0.5 micrograms.kg-1.h-1) were also measured before and after vagotomy. Vagotomy decreased basal and postprandial somatostatin levels and reduced the somatostatin responses to feeding during the first 30-min period following the ingestion of the meal but not during subsequent periods. Bombesin-induced somatostatin release was increased after vagotomy. Atropine decreased the somatostatin responses to the meal before and after vagotomy. Cimetidine had no significant effect. These studies suggest that, in conscious dogs, somatostatin released into the circulation is partly under vagal control and that, as for gastrin release, vagal pathways for stimulation and inhibition are present. Our studies also suggest that cholinergic mechanisms are involved in the control of postprandial somatostatin release.

Animals↗
PubMed1986

Effect of sham feeding on gastric emptying of liquids in dogs.

The effects of sham feeding and of cimetidine, an inhibitor of gastric acid secretion, used alone or in combination on the gastric emptying of liquids were studied in four dogs fitted with a gastric fistula and a Komarov esophagostomy. Gastric emptying of a 290-ml water meal was slowed by sham feeding but not by cimetidine. Our experiments indicate that, in dogs, sham feeding slows gastric emptying of liquids by a mechanism independent of the acid secretion induced by vagal stimulation.

Animals↗
PubMed1986

Influence of the stimulation state of the parietal cells on the inhibitory effect of omeprazole on gastric acid secretion in dogs.

The relationship between the stimulation state of the parietal cells and the gastric antisecretory properties of omeprazole has been evaluated in dogs with gastric fistulas maximally stimulated with pentagastrin. Intravenous administration of omeprazole (5 mumol/kg) 4 h before the start of stimulation with pentagastrin inhibited the acid response by 71%. This inhibition was prevented when omeprazole was given during an infusion of somatostatin at a dose that completely inhibited acid secretion. When given 18 h before stimulation with pentagastrin, omeprazole inhibited the acid response by 50%. This inhibitory effect was almost completely suppressed when omeprazole was administered during an infusion of somatostatin or after the administration of cimetidine, and was increased when omeprazole was given during an infusion of pentagastrin. These data indicate that the inhibitory effect of omeprazole given by rapid intravenous injection is related to the activity of the parietal cells at the moment of administration of the drug. They suggest that, in the intact animal as well as in the isolated gastric glands, the uptake of omeprazole by the parietal cells is related to the stimulation state of these cells.

Animals↗
PubMed1985

Presence of helodermin-like peptides of the VIP-secretin family in mammalian salivary glands and saliva.

Helodermin is a biologically active peptide isolated from the venom of the Gila monster lizard (Heloderma suspectum) whose structure is related to that of vasoactive intestinal peptide and secretin. Using a specific radioimmunoassay based on antisera prepared by immunizing rabbits with natural helodermin, we demonstrated the presence of helodermin-like material in mammalian salivary glands, including parotid, submaxillary and sublingual glands from rat and dog, and parotid and submaxillary glands from man. All helodermin-like materials had an apparent molecular mass of 4-12 kDa. Dog saliva, collected after pilocarpine stimulation, revealed similar immunoreactivity with a major component around 6 kDa.

Amino Acid Sequence↗
PubMed1985

Immunoreactive helodermin-like peptides in rat: a new class of mammalian neuropeptides related to secretin and VIP.

Helodermin is a peptide from the venom of the lizard Heloderma suspectum (Gila Monster) showing a high degree of sequence similarity with VIP, PHI and secretin in its N-terminal moiety. The present data support the presence of peptide(s) closely related to helodermin in the brain, gut and salivary glands of rat. In our radioimmunoassays, we routinely used one of the three specific antisera obtained from rabbits that were immunized against lizard helodermin coupled to bovine serum albumin with carbodiimide. Heat- and acid-stable immunoreactive helodermin-like material was more abundant in striatum, hippocampus and anterior pituitary than in cerebral cortex and hypothalamus. High levels of helodermin-like material were also present in salivary glands, duodenum and jejunum. When submitted to gel permeation chromatography on a TSK-G 2000 SW column, the apparent molecular radius of most of the immunoreactive material ranged from 6 to 12 KDa.

Animals↗
PubMed1985

Alanine turnover in normal and diabetic dogs.

The rate of turnover of alanine was determined in normal and insulin-deprived pancreatectomized dogs using a primed constant infusion of U-14 C-alanine. In the diabetic group, alanine levels and turnover rates were closely correlated suggesting that alanine production is a major determinant of its concentration. Alanine metabolism varied according to the degree of hyperglycaemia: when glucose levels were less than 22 mmol/l, alanine fluxes and concentrations remained normal as observed in previously published studies. In contrast, when glucose levels exceeded 25 mmol/l, alanine concentrations and fluxes tended to be markedly elevated (up to 4-5 times the normal values). This finding suggests that in severely hyperglycaemic animals in which hepatic glucose production is likely to be strikingly elevated, an excessive rate of transport of alanine from muscle to the liver might contribute to the accelerated rate of gluconeogenesis.

Alanine↗
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↗
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

[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↗