N-ethylmaleimide antagonizes stress-induced gastric ulcers in rats

Summary N-ethylmaleimide (NEM) 10 or 25 mg/kg b.wt, given s.c. 20 min beforehand, dose-dependently and significantly antagonizes the severity of gastric glandular ulcers produced by restraint at 4°C (stress) for 2 h. These findings suggest that reduced activity of endogenous nonprotein sulfhydryl substances in gastric tissue does not worsen stress-induced ulceration in rat stomachs, unlike the deleterious effect its depletion is claimed to have on ethanol-evoked gastric mucosal damage. Thus, decreased SH activity appears not to play a role in the aetiology of mucosal ulcers due to stress.     

The effect of nicotine on ethanol-induced gastric ulcers in rats

Summary Nicotine, in concentrations of 5 and 25 g/ml drinking water, given ad libitum for 10 days, dose-dependently increased lesion formation and worsened ethanol-induced ulceration in rat stomachs. Daily fluid intake and b.wt gain were not adversely affected by nicotine pretreatment.The authors are grateful to Mr C.T. Luk for his skilled technical assistance.     

Nitric oxide inhibition intensifies cold-restraint induced gastric ulcers in rats

Treatment 20 min beforehand with an inhibitor of nitric oxide (NO) synthesis, N^W-nitro-l-arginine methyl ester (L-NAME) (12.5, 25, 50 or 100 mg/kg, s.c.), dose-dependently intensified gastric glandular mucosal ulceration produced by cold-restraint stress. Hexamethonium (20 mg/kg) or atropine (1 mg/kg) pretreatment s.c. 20 min before stress strongly antagonised stress-evoked ulceration, as well as the ulcer-potentiating effects of L-NAME when either cholinoceptor antagonist was given concurrently with the NO inhibitor. Stress-induced mast cell degranulation was not worsened by L-NAME pretreatment. The findings suggest that NO could confer partial protection against stress-induced gastric ulcer formation; its activity is triggered off by the ulcerogenic mechanism of stress.     

The effect of nicotine on ethanol-induced gastric ulcers in rats

Nicotine, in concentrations of 5 and 25 micrograms/ml drinking water, given ad libitum for 10 days, dose-dependently increased lesion formation and worsened ethanol-induced ulceration in rat stomachs. Daily fluid intake and b.wt gain were not adversely affected by nicotine pretreatment.     

The influence of thenalidine on reserpine- and serotonin-induced gastric ulcers in rats

Zusammenfassung Die Vorbehandlung mit Thenalidin (Sandosten) führt zur Verminderung der mit Serotonin hervorgerufenen hämorrhagischen Erosionen im Magen der Ratten. Thenalidin zeigt einen Effekt auf das mit Reserpin bewirkte Magengeschwür und verstärkt die Vormagengeschwürbildung bei den Ratten.

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Trademark employed by Sandoz Pharmaceuticals is Sandosten.     

Effect of subdiaphragmatic vagotomy on production of gastric ulcers in pylorus-ligated albino rats

Summary A reduction in volume and free and total acidity of gastric content was noted along with reduction in ulcer index, with a shift of the site of ulceration from fundus to the glandular part of stomach, following vagotomy in pylorus-ligated rats. Low volume and acidity explains the absence of ulcers in the fundus, but the increased involvement of glandular part in ulceration is possibly due to weakening of the mucosal barrier following vagotomy.     

The influence of chronic nicotine treatment on stress-induced gastric ulceration and emptying rate in rats

Ten-day treatment with nicotine, (5, 25 or 50 g/ml drinking water) dose-dependently intensified gastric ulceration induced by cold-restraint, and emptying rate. Stomach contractions produced by graded doses of bethanechol i.v. were elevated further by nicotine treatment. It is suggested that chronic nicotine administration produces hypersensitivity of the gastric muscarinic receptors; stomach hypermotility contributes to the ulcer-worsening action of the alkaloid     

The influence of peripheral or central administration of ondansetron on stress-induced gastric ulceration in rats

Ondansetron (0.08, 0.15 or 0.3 mg/kg) injected s.c., every 12h with the fourth dose given 0.5 h before experiments, dose-dependently lessened gastric glandular mucosal ulceration produced by cold-restraint stress for 2h. When given intracerebrally (i.c.) (0.1, 0.5 or 1g), using the same treatment regimen, infusion of ondansetron 1 g into the nucleus amygdaloideus centralis decreased stress-evoked ulcers; in contrast, injection of the same dose into the nucleus accumbens intensified these lesions. The associated stress-induced stomach wall mast cell degranulation was unaffected by all s.c. or i.c. doses of ondansetron. Pretreatment with disodium cromoglycate i.p. alone, or concurrently with ondansetron s.c., prevented not only ulceration but also mast cell degranulation. 5-Hydroxytryptamine₃ receptor antagonism appears to inhibit stress-evoked ulcers mainly by blocking the peripheral effects of the amine after its release from the gastric mucosal mast cells.     

Effect of subdiaphragmatic vagotomy on production of gastric ulcers in pylorus-ligated albino rats.

A reduction in volume and free and total acidity of gastric content was noted along with reduction in ulcer index, with a shift of the site of ulceration from fundus to the glandular part of the stomach, following vagotomy in pylorus-ligated rats. Low volume and acidity explains the absence of ulcers in the fundus, but the increased involvement of glandular part in ulceration is possibly due to weakening of the mucosal barrier following vagotomy.     

The influence of chronic nicotine treatment on stress-induced gastric ulceration and emptying rate in rats.

Ten-day treatment with nicotine (5, 25 or 50 micrograms/ml drinking water) dose-dependently intensified gastric ulceration induced by cold-restraint, and emptying rate. Stomach contractions produced by graded doses of bethanechol i.v. were elevated further by nicotine treatment. It is suggested that chronic nicotine administration produces hypersensitivity of the gastric muscarinic receptors; stomach hypermotility contributes to the ulcer-worsening action of the alkaloid.     

Running activity and gastric ulcers in the rat

Zusammenfassung Nachweis von Magenulzerationen und Magenerosionen bei Albinoratten nach bestimmter Fütterung und nachherigem Laufkäfig-Aufenthalt. Problem der Stressulzeration und die Rolle der Diät werden erörtert.

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The authors appreciate the excellent technical assistance of Messrs.J. Krebs andJ. Tomlinson     

Depression of experimental gastric ulcers and acute pancreatitis in rats treated by 5-azacytosine, 5-azacytidine and their N-methyl derivatives

5-Azacytosine, 1-methyl-5-azacytosine and 5-azacytidine administered to rats with a ligated pylorus block gastric secretion, gastric acidity, the extent of hemorrhage and the number and size of gastric defects. The same drugs also depress the development of experimental acute pancreatitis mediated in rats by interstitial administration of 7.5% natrium cholate into the pancreas in vivo. The drugs affected the amount of abdominal fluid and 6 h after the treatment the pathological changes were significantly decreased.     

Depression of experimental gastric ulcers and acute pancreatitis in rats treated by 5-azacytosine, 5-azacytidine and their N-methyl derivatives

Summary 5-Azacytosine, 1-methyl-5-azacytosine and 5-azacytidine administered to rats with a ligated pylorus block gastric secretion, gastric acidity, the extent of hemorrhage and the number and size of gastric defects. The same drugs also depress the development of experimental acute pancreatitis mediated in rats by interstitial administration of 7.5% natrium cholate into the pancreas in vivo. The drugs affected the amount of abdominal fluid and 6 h after the treatment the pathological changes were significantly decreased.     

Nicotine and ascorbic acid effects on cold-restraint ulcers in rats

Summary Rats were orally administered 1-ascorbic acid, nicotine, 1-ascorbic acid and nicotine, or distilled water for 10 days. Following this treatment they were fasted for 24 h and then restrained in a cold environment for 2h. Nicotine alone produced significantly more gastric ulcers than any other treatment. 1-Ascorbic acid increased ulceration relative to controls. The combined effects of 1-ascorbic acid and nicotine resulted in reduced ulcer incidence and severity. It appears that 1-ascorbic acid and nicotine do not act synergistically to augment stress-induced gastric ulcer. Supported by Natural Sciences and Engineering Research Council of Canada grant No. A 6312.     

Influence of iproniazid pretreatment on formation of gastric ulcers by reserpine in the rat

Résumé Chez le rat à pylore lié, la réserpine (5 mg/kg) provoque l'apparition précoce d'ulcérations gastriques. Ce phénomène fait défaut si les rats ont été traités préalablement par l'iproniazide, un inhibiteur de la monoamino-oxydase.      

The effect of hog gastrin on gastric secretion in chronic gastric fistula rats

Résumé L'action de la gastrine de porc a été étudiée chez des rats mâles munis de fistules gastriques. La gastrine était injectée par voie s.c. à des doses de 1–2 ml: 1 ml équivalant à l'activité de 10 g de muqueuse de porc. Le volume de suc gastrique, le volume de suc gastrique par 100 g, l'acidité totale et le débit d'acide accusèrent une pointe dans la première h, alors que la concentration en acide atteignit son maximum vers la troisième h. Le débit de la pepsine diminua entre la troisième et la cinquième h et augmenta légèrement entre la cinquième et la sixième h.

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This research was supported in part by grants from the National Science Foundation (No. GB 6105) and from the AMA ERF, to J. H. T. — Dr.Robitscher of Ayerst Laboratories kindly supplied the ICI-50123.