Pathophysiology and pathogenesis of acute gastric mucosal lesions after hypothermic restraint stress in rats

Murakami, Motonobu; Lam, Shiu Kum; Inada, Masami; Miyake, Teruki

doi:10.1016/0016-5085(85)90133-7

Cited by 107 publications

(59 citation statements)

References 18 publications

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“…Decreased gastric mucosal blood flow has been reported as one important factor related to lesion formation induced by restraint and water-immersion stress (11,12). In the present study, we can not discuss the correlation between the initial surface epithelial cell damage and decreased gastric mucosal blood flow in stressed rats.…”

Section: Discussioncontrasting

confidence: 59%

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Surface epithelial cell damage induced by restraint and water-immersion stress in rats. Effects of 16,16-dimethyl prostaglandin E2 on stress-induced gastric lesions.

et al. 1987

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Abstract-The time-course of gastric mucosal surface epithelial cell damage and macroscopically visible lesions in response to restraint and water-immersion stress (22°C) in rats was examined, and the effects on it of 16,16-dimethyl prostaglandin E 2 (dmPGE2) were compared with those of papaverine, timoprazole and atropine.The stress produced surface epithelial cell damage prior to visible lesion, the former increasing in severity with time and reaching a plateau 60 min later, by which time exfoliation of surface epithelial cells was observable along the mucosal folds. In contrast, macroscopically visible lesions appeared 2 hr after stress, and severity continued to increase with time. Pretreatment injections (s.c.) of dmPGE2 (3, 30 icg/kg), papaverine (100 mg/kg) and atropine (1 mg/kg) protected the surface cells against stress (1 hr)-induced damage, and inhibited visible lesion formation after 4 hr stress. Timoprazole (30 mg/kg, s.c.) did not protect the surface cells, but did markedly inhibit visible lesion formation. dmPGE2, papaverine and atropine, but not timoprazole, inhibited stress-induced increases in gastric contractions. dmPGE2, timoprazole and atropine, but not papaverine, inhibited acid secretion in stress-conditions. These results indicated that stress induced damage to the gastric mucosa within 1 hr due to increased gastric contractions, and the surface epithelial cell damage developed into macroscopically visible lesions in the presence of acid, and that dmPGE2 protected the surface epithelium against stress-induced damage probably by inhibiting gastric contractions.

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Section: Discussioncontrasting

confidence: 59%

“…Changes in gastric secretion (7,8), abnormal gastric motility (9,10), and disturbance of gastric mucosal microcircu lation (11,12) have been implicated as underlying pathogenetic mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Surface epithelial cell damage induced by restraint and water-immersion stress in rats. Effects of 16,16-dimethyl prostaglandin E2 on stress-induced gastric lesions.

et al. 1987

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“…The hypothermic restraint-stress model used here increases acid secretion and decreases the gastric mucosal pH (Murakami et al 1985). Brozozowski et al (2000) observed that the exposure of rats to 3.5 h of stress induced by cold and restraint produced gastric lesions, and that this effect was accompanied by a decrease in prostaglandin (PGE 2 ) generation and a marked fall in gastric blood flow.…”

Section: Resultsmentioning

confidence: 92%

Antiulcerogenic activity of Indigofera truxillensis Kunth

et al. 2006

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Cola-Miranda, M; Barbastefano, V.; Hiruma-Lima, C.A.; Calvo, T.R.; Vilegas, W. and Brito, A.R.M.S. Antiulcerogenic activity of Indigofera truxillensis Kunth. Biota Neotrop. Sep/Dec 2006 vol. 6, no. 3 http://www.biotaneotropica.org.br/v6n3/ pt/abstract?article+bn01006032006 ISSN 1676-0611The genus Indigofera (Fabaceae) is used in folk medicine to treat gastrointestinal pain. In this study, we investigated the antiulcerogenic properties of Indigofera truxillensis Kunth. Oral administration of MeOH extract did not produce any signals of acute toxicity. The antiulcerogenic activity was assessed in different models of acute gastric ulcers (100% ethanol, piroxicam 30 mg.kg -1 , hypothermic restraint stress and pylorus ligature) in mice and rats. The animals were treated with the drugs lanzoprazole (30 mg.kg -1 ) or cimetidine (100 mg.kg -1 ) as positive controls depending on the performed model. In another experiment with ethanol-induced ulcers in rats, N-ethylmaleimide (NEM), a sulfhydryl group blocker, was also used. The MeOH extract, at doses of 250, 500 and 1000 mg.kg -1 , inhibited the gastric lesions in all experiments: a) by 62%, 69% and 32%, respectively, in piroxicam-induced lesions, b) by 43%, 71% and 98%, in ethanol-induced lesions, c) by 69%, 64 and 89%, in hypothermic-restraint stress-induced lesions, d) by 73%, 82% and 84%, in pylorus ligature lesions. Significant changes in the total gastric acid levels were also found after intraduodenal administration of the MeOH extract in the ligated pylorus model. Pre treatment with NEM reduced partially the antiulcerogenic activity of the MeOH extract in ethanolinduced gastric lesions. This result indicates an increase in the levels of non-protein sulfhydryl groups by MeOH extract in the gastric mucosa. These results indicate that the MeOH extract has antisecretory and citoprotective effects that may be related to the presence of flavonoids detected by phytochemical analysis. O gênero Indigofera (Fabaceae) é utilizado na medicina tradicional para distúrbios gastrintestinais. Em nosso trabalho foi investigada a propriedade antiulcerogênica da Indigofera truxillensis Kunth. A administração oral do extrato metanólico (MeOH) não produziu efeitos tóxicos. A atividade antiulcerogênica foi avaliada em diferentes modelos agudos de úlcera gástrica (etanol 100%, piroxicam 30 mg.kg -1 , estresse por retenção e frio e ligadura do piloro) em camundongos e ratos. Os animais foram tratados com lansoprazol (30 mg.kg -1 ) ou cimetidina (100 mg.kg -1 ), que foram utilizados como controle positivo dependendo do modelo testado. Em outro experimento com úlcera induzida por etanol em ratos, N-etilmaleimida (NEM), um bloqueador dos compostos sulfidríla, também foi utilizado. O extrato metanólico, nas doses de 250, 500 e 1000 mg.kg -1 , inibiu significativamente as lesões gástricas em todos os experimentos: a) 62%, 69% e 32%, respectivamente, nas lesões gástricas induzidas por piroxicam, b) 43%, 71% e 98%, nas lesões gástricas induzidas por etanol, c) 69%, 64% e 89%, nas lesões ...

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“…On the other hand, indomethacin-induced ulcers seemed to involve inhibition of gastric prostaglandins derived mainly via COX-1, with some involvement of COX-2 (El-Bayer et al, 1985;Beck et al, 1990;Iseki, 1995;Wallace, 1997;Schmassmann et al, 1998). Stress-induced ulcers are believed to result from an increase in gastric acid secretion (Kitagawa et al, 1979;Marrone, 1984), a decrease in gastric PGE 2 production (Moody, 1976;Arakawa et al, 1981) and disturbed microcirculation in the gastric mucosa (Murakami et al, 1985). Proanthocyanidins are shown to suppress COX-2 enzyme (Yokozawa et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

Some pharmacological actions of Myrica rubra part 1: Effect on experimentally-induced gastric ulcers, inflammation and haemorrhoids in rats

AlAjmi¹

2013

Afr. J. Pharm. Pharmacol.

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Pathophysiology and pathogenesis of acute gastric mucosal lesions after hypothermic restraint stress in rats

Cited by 107 publications

References 18 publications

Surface epithelial cell damage induced by restraint and water-immersion stress in rats. Effects of 16,16-dimethyl prostaglandin E2 on stress-induced gastric lesions.

Surface epithelial cell damage induced by restraint and water-immersion stress in rats. Effects of 16,16-dimethyl prostaglandin E2 on stress-induced gastric lesions.

Antiulcerogenic activity of Indigofera truxillensis Kunth

Some pharmacological actions of Myrica rubra part 1: Effect on experimentally-induced gastric ulcers, inflammation and haemorrhoids in rats

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