Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In patients with peptic ulceration, both vagal stimulation by insulin hypoglycaemia and stimulation by pentagastrin cause pepsin 1 to be secreted into gastric juice. There is a secretory threshold for pepsin 1, below which only pepsins 3 and 5 are secreted. Pepsin 1 accounts for an increasing proportion of the total peptic activity/ml of gastric juice as the total activity increases. Higher concentrations of pepsin 1 in the basal gastric secretion occurred significantly more frequently in patients with duodenal ulcer than with gastric ulcer. In these patients there may be an increased 'background' secretory drive.
 ...
PMID:Pepsin 1 secretion in chronic peptic ulceration. 677 16

Factors implicated in the pathogenesis of gastric ulcer were studied simultaneously in seven patients with strictly defined type 1 gastric ulcer (single benign ulcer above the incisura of the stomach) and in six healthy controls. After ingestion of an ordinary solid-liquid meal, patients with gastric ulcer demonstrated gastric hyposecretion of acid, pepsin, and water; delayed gastric emptying of solids with normal emptying of liquids; and increased intragastric concentrations of bile acids. These functional abnormalities appear to be interrelated. Metoclopramide, administered orally in a double-blind fashion, ameliorated the defect in the emptying of solids and the high concentrations of bile acid in the gastric contents. The ability of this drug to break this interdependent cycle suggests the need for further clinical investigation.
 ...
PMID:Dysfunctions of the stomach with gastric ulceration. 677 31

The effects of fundic vagotomy on acid and pepsin secretion in 12 patients (10 males, two females; nine duodenal ulcer, three gastric ulcer) were studied using a pentagastrin dose response before and after Vagotomy. In the intact stage H, Cl, and pepsin output all had the same ED50, 120-127 pmol/kg/h. Vagotomy reduced basal output of acid by 78%, Cl- by 50%, and pepsin by 62%. Postvagotomy basal outputs were not related to preoperative levels, while maximum acid output was reduced by an average of 35%, proportionally to the preoperative output (r = 0.94). Vagotomy uncompetitively (ED50 increase, Vmax decrease) inhibited the pentagastrin dose response of acid, chloride, and pepsin output. Postoperatively, a six-fold greater dose of pentagastrin (450 vs 76 pmol/kg/h) was required to stimulate acid to 50% of its preoperative maximum output. For pepsin secretion the increase was 12-fold (185 vs 15 pmol/kg/h). In five of the nine duodenal ulcer patients pentagastrin dose responses were repeated with a background infusion of urecholine, 20 micrograms/kg/h. Urecholine increased basal and peak acid, pepsin, and chloride outputs, and the ratio of basal: maximal almost to prevagotomy levels; it also restored the sensitivity to pentagastrin. Serum gastrin was not significantly changed by urecholine or by vagotomy. We conclude that the level of basal acid and pepsin secretion in ulcer patients, which is largely eliminated by vagotomy, is dependent on the vagus and not on serum gastrin. The effects of vagotomy are functional, are due to cholinergic withdrawal, and usually can be restored by cholinergic replacement.
 ...
PMID:Effects of fundic vagotomy and cholinergic replacement on pentagastrin dose responsive gastric acid and pepsin secretion in man. 680 59

14C-Sucralfate, a basic aluminum salt of 14C-sucrose sulfate, or potassium 14C-sucrose sulfate was administered orally to rats with acetic acid-induced gastric ulcer. The radioactivities representing specific binding of the sucrose sulfate moiety were found significantly higher in ulcer sections of the stomach, with the mean within-animal ulcer/non-ulcer ratio attaining 6, 7, 12 and 2.5, respectively, at 1, 3, 6 and 24 h after 14C-sucralfate administration. Microautoradiography provided direct in vivo evidence for binding of the 14C-sucrose sulfate moiety to exuded proteins resulting in effect in formation of a pepsin-resistant barrier over the surface of an ulcer crater. No comparable findings were obtained in the area of normal mucosa. The administration of 14C-sucralfate was associated with much greater and longer-sustained binding to the ulcer lesion and retention in the stomach and duodenum than simple administration of the soluble potassium salt. These findings not only demonstrate therapeutically significant effects of basic aluminum compoundation but also substantiate likely differences from pepsin inhibitors such as amylopectin sulfate in terms of presence or absence of adhesiveness, local barrier effects, and long duration of actions.
 ...
PMID:Selective binding of sucralfate to ulcer lesion. II. Experiments in rats with gastric ulcer receiving 14C-sucralfate or potassium 14C-sucrose sulfate. 689 77

Calcitonin (CT) inhibits basal and pentagastrin stimulated gastric acid and pepsin secretion by 60 to 70% when CT is infused over a short period of time. Vagal and histamine-mediated stimulations are less diminished. A long-term infusion of CT inhibits persitently basal and pentagastrin-stimulated acid and pepsin secretion over more than 24 hours in patients with duodenal ulcer, stress bleeding and Zollinger-Ellison-Syndrome. To date, the therapeutic efficiency of CT in gastroduodenal bleeding has not been evaluated in a controlled trial. CT inhibits gastric secretion also after oral application. In an endoscopically controlled double blind trial we were not able to demonstrate a significant benefit of oral CT in patients with gastric ulcer. In ulcer bleeding CT does not apear reasonable in comparison with histamine-H2-receptor antagonists which apparently is more efficient and less costly.
 ...
PMID:[Theoretical and practical implications of calcitonin therapy in gastroduodenal ulcer]. 699 53

Sodium polyacrylate (PANa) is a water-soluble, high-molecular compound, and its aqueous solution shows a very high viscosity and stringiness. In the present study, preventive effects of PANa on three kinds of esophageal lesions induced by gastric juice were examined in comparison with those of aceglutamide aluminum and sodium alginate. The influences of PANa on gastric contents were also studied. The preventive effect of PANa given intraesophageally on esophageal lesions induced by the intraesophageal application of gastric juice was more potent than aceglutamide aluminum and sodium alginate. Oral administration of PANa inhibited the formation of esophageal ulcer by pylorus ligation more markedly than aceglutamide aluminum, whereas sodium alginate had no effect in a high dose of 500 mg/kg. In preventing gastric ulcer which occurred simultaneously with the esophageal ulcer after the pylorus ligation, aceglutamide aluminum was most potent, and PANa was as potent as sodium alginate. Oral administration of PANa showed a more protective effect than aceglutamide aluminum on the esophageal ulceration induced by the simultaneous ligations of the pylorus and limiting ridge, whereas sodium alginate in a high dose of 500 mg/kg had little effect on the ulcer formation. PANa caused only a slight increase in the pH of gastric juice and a slight decrease in pepsin activity. From the results, it may be concluded that PANa showed an antiulcerogenic activity mainly due to its mucosa covering action against gastric juice.
 ...
PMID:Effects of sodium polyacrylate (PANa) on acute esophagitis by gastric juice in rats. 710 49

The effects of three typical antisecretory agents: cimetidine, atropine and prostaglandin E2 were compared on an acute rat gastric ulcer model which consisted of perfusing the stomach continuously, at a high intraluminal pressure (120 mm H2O), with a simulated gastric juice (0.1 M HCl plus 600 mg pepsin/l). As the acid and pepsin are given exogenously the inhibitory action of the antisecretory drugs is obviated in this model. Cimetidine and atropine failed to reduce gastric erosions, whereas prostaglandin E2 markedly reduced the severity of the mucosal lesions with respect to control values. Long-term treatment with cimetidine also failed to increase the resistance of the gastric mucosa to the digestive action of the artificial gastric juice. These findings indicate that only prostaglandin E2 is cytoprotective and do not support the view that anticholinergics or histamine H2-receptor antagonists have a cytoprotective role on the cells of the gastric mucosa.
 ...
PMID:Effects of cimetidine, atropine and prostaglandin E2 on rat mucosal erosions produced by intragastric distension. 744 34

Gastroduodenal ulcer disease comprises a heterogeneous group of different diseases resulting uniformly in a mucosal defect reaching beyond the muscularis mucosae. Consequently, a single unifying pathogenesis of ulcer disease does not exist but only a rather general concept that ulcers develop when mucosa-injuring factors outweigh the mucosa-protecting factors. According to this concept, ulcers develop within a broad range of different possibilities in the relation of mucosa-injuring factors to impaired mucosal protection. The main histological and physiological elements for the understanding of peptic ulcer disease are briefly summarized, followed by a short survey of the important known 'traditional' abnormalities of possible pathogenetic importance in duodenal and gastric ulcer patients. Gastroduodenal ulcer disease represents a typical example of a multifactorial disease, where different combinations of both hereditary and environmental factors produce the same morphological lesion. By far the most exciting data of the last ten years originate from the still increasing understanding of the role of Helicobacter pylori in gastroduodenal ulcer disease. The most important evidence and hypotheses are presented of how and where Helicobacter pylori is or could be involved in the complicated pathogenetic network of ulcer disease. The infection of gastric epithelium by Helicobacter pylori has become the second main factor besides acid/pepsin in the pathogenesis of ulcer disease. Beside the improved insights in ulcer pathogenesis, the translation of the new data into clinical medicine has led and will lead to remarkable progress. Most important: a causal therapy of ulcer disease has become available in contrast to the so far practiced sole symptomatic treatment of single ulcer episodes. What has treatment of single ulcer episodes. What has been a domain of ulcer surgery has come into reach of drug therapy.
 ...
PMID:[Gastroduodenal ulcer disease: update on pathogenesis]. 779 67

The present study was carried out to investigate the central effects of pancreatic polypeptide on gastric secretion and gastric ulcer formation in conscious rats. Intracisternal injection of rat pancreatic polypeptide (62.5, 250, and 1000 ng/rat) into pylorus-ligated rats resulted in a dose-dependent stimulation of gastric acid and pepsin secretion. In contrast, intraperitoneal injection of even higher doses of pancreatic polypeptide (250, 1000, and 2500 ng/rat) failed to increase gastric secretion. This stimulatory effect of centrally administered pancreatic polypeptide was completely blocked by vagotomy and by pretreatment with atropine. Intracisternal injection of PP (500-2000 ng/rat) dose-dependently increased the severity of gastric lesions induced by 2-deoxy-D-glucose or indomethacin. In contrast, intraperitoneal injection of PP failed to increase the severity of the gastric lesions induced by 2-deoxy-D-glucose or indomethacin. These results indicate that pancreatic polypeptide is capable of acting centrally in the brain to stimulate gastric acid and pepsin secretion through a vagal, muscarinic pathway and in so doing exerts an ulcerogenic action on the gastric mucosa.
 ...
PMID:Stimulation of gastric secretion and enhanced gastric mucosal damage following central administration of pancreatic polypeptide (PP) in rats. 795 9

Helicobacter pylori (Hp) infection is thought to play an important role in for the pathogenesis of atrophic gastritis and even gastric carcinoma. The ratio of Pepsinogen I/II (P I/II) also shows good correlation with atrophic gastritis and gastric ulcer. Since many hemodialysis (HD) and renal transplantation patients suffer from gastrointestinal problems, we investigated the importance of Hp infection and P I/II in these patients. Serum Hp IgG was measured by EIA. Pepsinogen titer was measured with antipepsinogen antibody-bearing beads and anti-pepsinogen antibody. Hp positive HD patients accounted for 50.7% of the subjects. Of the renal transplantation patients, 23.5% were positive with lower values than the HD patients. The value of P I/II in all patients with a high Hp positive titer also was low (under 3). In conclusion, serum IgG antibody to Hp and P I/II exhibit good correlation and both are useful for the diagnosis of atrophic gastritis in chronic renal failure.
 ...
PMID:[Importance of Helicobacter pylori infection and pepsinogen titer in hemodialysis and renal transplantation patients in Japan]. 807 24


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>