Scandinavian journal of gastroenterology. Supplement
-
Scand. J. Gastroenterol. Suppl. · Jan 1984
Effect of pentobarbital anesthesia and bile acids on cysteamine-induced duodenal and gastric ulcers in rats.
Cysteamine given three times within 8 h produced severe duodenal and gastric ulcers in female SIV rats. A pentobarbital anesthesia during the first 10 h prevented gastric ulcer formation without affecting duodenal ulcer. ⋯ Treatment with somatostatin significantly reduced the intensity of duodenal ulcer. The inhibition of cysteamine-induced gastric ulcer formation by pentobarbital does not seem to be due to a possible inhibition of duodenogastric reflux but more likely to an inhibition of central nervous stress reactions by anesthesia.
-
Scand. J. Gastroenterol. Suppl. · Jan 1984
Comparative StudyDiversion of bile and pancreatic secretion in the rat and its effect on cysteamine-induced duodenal and peptic ulcer development under maximal acid secretion.
In this investigation we assess whether diversion of bile and pancreatic secretion protects rats from ulceration under maximal acid secretion as it does in cysteamine-induced ulcers. The rats were divided into a cysteamine-group (Cy) comprising 16 rats and a secretagogue group (PC) with 18 white male rats. Half of the animals of each group were submitted to the diversion-operation (division of the duodenum distally from the pylorus, jejuno-duodenostomy and entero-y-anastomosis), Cy2 and PC2 respectively. ⋯ Furthermore in PC1 group 34 gastric ulcers were found in 7 rats and only 4 ulcers in the PC2 group. It is therefore concluded, that the diversion operation provided protection against cysteamine-induced duodenal ulcers (p less than 0.01) and ulcer formation under maximal acid stimulation in the duodenum (p less than 0.02) as well as in the rat stomachs (p less than 0.05). In the PC group the restraint haltering of the animals promoted presumably a stress situation with bile reflux in the non-operated whereas in the operated animals (PC2) reflux did not occur.
-
Scand. J. Gastroenterol. Suppl. · Jan 1984
Role of local secretory and motility changes in the pathogenesis of experimental duodenal ulcer.
Changes in gastric acid and pepsin secretions do not fully account for the duodenal ulcerogenic effect of cysteamine or propionitrile in the rat. We investigated the role of pancreatic and biliary secretions as well as motility changes in the duodenum. Bypass of bile to the jejunum and/or ablation of pancreatic secretion or drainage of these secretions through chronic duodenal fistula aggravated the cysteamine-induced duodenal ulcers. ⋯ An increased and dopamine-sensitive myoelectric activity caused by cysteamine or propionitrile was recorded in the proximal duodenum, indicating a state of hypermotility. Indeed, a decreased quantity of bilirubin was recovered through the chronic fistula in the proximal duodenum, suggesting an impaired delivery of bile to the ulcer area after cysteamine administration. Thus, duodenal hypermotility probably prevents the proper mix and neutralization of gastric acid and duodenal (mucosal, biliary and pancreatic) secretions, predisposing to ulceration in the proximal duodenum.
-
Scand. J. Gastroenterol. Suppl. · Jan 1984
The role of bile salts in cysteamine-induced duodenal ulcer in the rat and the ulceroprotective property of lysolecithin.
Cysteamine induces duodenal ulcers in rats, but bile diversion inhibits ulcer formation. Since lysolecithin inhibits stress ulceration in rats, it is assessed now whether lysolecithin inhibits cysteamine-induced ulcers, too. Male rats were operated: division of the duodenum distally to the pylorus, duodenojejunostomy. Roux-en-Y duodenojejunostomy. 4 groups comprising 10 animals. Drinking solution for group 1, 3 and 4: Na taurocholate and glycocholic acid (5 mmol/l). For group 2 addition of 0.2 mmol/l lysolecithin. Cysteamine-HCl (10%) twice subcutaneously on the 19th day in group 1, 3 and 4, isotonic NaCl in group 2. In group four 1 ml lysolecithin per gastric tube 1 h before cysteamine. ⋯ Lysolecithin, a substance produced during fat digestion, exerted an ulceroprotective property (lyso-protection) under experimental conditions, as shown here for the first time, to the author's knowledge. The enhancement of cysteamine-induced duodenal ulcer development by bile salts is again documented.
-
Scand. J. Gastroenterol. Suppl. · Jan 1984
Enhancement of duodenal and jejunal ulceration by histamine-induced gastric hypersecretion in dogs with diversion of duodenal contents.
In a previous investigation deviation of duodenal contents protected rats significantly from the development of peptic ulceration under maximal acid secretion. We have now assessed the effect of diversion of duodenal contents in dogs submitted to the same operative procedure under histamine-induced hypersecretion. Six mongrel dogs underwent the following procedure: A two cm duodenal segment was left adjacent to the intact pylorus, proximal jejunum anastomosed to this segment and a Roux-en-Y duodeno-jejunostomy performed. ⋯ It was concluded that the diversion of duodenal contents enhanced ulcer formation in dogs and that the model mimicked a Zollinger-Ellison Syndrome. Ulceration occurred in transitional or jejunal type of duodenal mucosa. No gastric lesions were found and this suggests that the diversionary procedure was an effective means of preventing bile from reaching the gastric mucosa.