The role of nitric oxide in the gastric acid secretion induced by ischemia–reperfusion in the pylorus-ligated rat

Tanaka, Junko; Yuda, Yasukatu; Inouye, Shigeharu; Yamakawa, Toshio

doi:10.1016/s0014-2999(01)01119-0

Cited by 27 publications

(16 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Tanaka et al [41] reported that both L -NAME as well as the iNOS inhibitor aminoguanidine increased gastric acid secretion under I/R conditions in rats and suggested that the suppression of acid secretion during I/R is partly mediated by NO produced in the infiltrating neutrophils. In the present study, however, neither of these agents had any effect on basal acid secretion in the mouse stomach.…”

Section: Discussionmentioning

confidence: 99%

Dual Action of Nitric Oxide in the Pathogenesis of Ischemia/Reperfusion-Induced Mucosal Injury in Mouse Stomach

et al. 2007

View full text Add to dashboard Cite

Aim: We investigated the roles of NO/NOS isoforms in the pathogenesis of ischemia/reperfusion (I/R)-induced gastric injury in mouse stomachs. Methods: Under urethane anesthesia, the celiac artery was clamped, and then reperfusion was established 30 min later by removal of the clamp. After a 60-min reperfusion, the stomach was examined for macroscopic lesions. Results: Following I/R, hemorrhagic lesions were generated in the mucosa, although ischemia alone caused no visible damage. Prior administration of L-NAME (a nonselective NOS inhibitor) significantly aggravated these lesions, in a L-arginine-inhibitable manner. By contrast, the selective iNOS inhibitor 1400W significantly prevented the occurrence of I/R-induced gastric lesions. The mucosal MPO activity was increased after I/R, and this response was enhanced and attenuated by prior administration of L-NAME and 1400W, respectively. Interestingly, the later treatment with L-NAME, given 10 min before reperfusion, significantly reduced the severity of the I/R-induced gastric damage, in a L-arginine-dependent manner. The expression of iNOS mRNA was up-regulated in the stomach following I/R, with an increase of mucosal NO content, and the NO production was significantly inhibited by both L-NAME and 1400W. Conclusion: Endogenous NO plays a dual role in the pathogenesis of IR-induced gastric damage; NO/cNOS is protective while NO/iNOS is proulcerogenic during I/R.

show abstract

Section: Discussionmentioning

confidence: 99%

Dual Action of Nitric Oxide in the Pathogenesis of Ischemia/Reperfusion-Induced Mucosal Injury in Mouse Stomach

et al. 2007

View full text Add to dashboard Cite

show abstract

“…It is known that gastric mucosal constitutive nitric oxide synthase (cNOS) regulates gastric mucus synthesis and secretion as well as gastric mucosal microcirculation. However, the overproduction of nitric oxide by leukocytes through the induction of iNOS activity has been recently found to play an important role in depressing gastric acid secretion and inducing gastric lesions on ischemia-reperfusion in the pylorus-ligated rat [13,14]. It has been also found that pretreatment with aminoguanidine, a selective iNOS inhibitor, prevents lesion formation in rats, although it augments the gastric acid output that is rendered to be depressed by ischemia-reperfusion [14].…”

Section: Discussionmentioning

confidence: 99%

“…However, the overproduction of nitric oxide by leukocytes through the induction of iNOS activity has been recently found to play an important role in depressing gastric acid secretion and inducing gastric lesions on ischemia-reperfusion in the pylorus-ligated rat [13,14]. It has been also found that pretreatment with aminoguanidine, a selective iNOS inhibitor, prevents lesion formation in rats, although it augments the gastric acid output that is rendered to be depressed by ischemia-reperfusion [14]. These findings, with the present results, suggest that curcumin at doses of more than 40 mg/kg partially attenuates the antiulcerogenic effect through the increase in acid secretion.…”

Section: Discussionmentioning

confidence: 99%

Preventive and curative effects of curcumin on the development of gastric inflammatory diseases in rats

et al. 2006

View full text Add to dashboard Cite

Preventive and curative effects of curcumin on experimental acute and chronic gastric ulcers were investigated to validate its clinical application on a remedy for peptic ulcer. Intraduodenal administration of curcumin, 5-20 mg/kg, inhibited gastric acid secretion in pylorus-ligated rats, and oral administration prevented ethanol-induced acute gastric mucosal lesions. Curcumin (20-80 mg/kg, p.o.) dose-dependently prevented both serotonin-induced gastric mucosal lesions and compound 48/80-induced gastric mucosal lesions in rats. Furthermore, oral administration of curcumin, 10-80 mg/kg, twice daily for 10 days, significantly accelerated the healing of acetic acid-induced chronic gastric ulcer and promoted mucosal regeneration in the ulcerated portion in a dose-related manner. Cimetidine prevented the formation of ethanol-induced gastric mucosal lesions, but not of serotonin-induced and compound 48/80-induced gastric mucosal lesions. Consecutive administration of cimetidine showed a marked acceleration in the healing of acetic acid-induced ulcer. Aminoguanidine, an inducible nitric oxide synthase (iNOS) inhibitor, showed anti-ulcerogenic effects similar to those oberved for curcumin. The present results indicate that curcumin exhibits gastric cytoprotection in the acute lesion models and ulcer healing promotion in the chronic ulcer model. The preventive and curative effects of curcumin might be due to an increase in the mucosal defensive mechanism through its antioxidant property and inhibition of NO or cytokine-mediated inflammation.

show abstract

“…The reason that L-arginine reduced gastric acid secretion might be due to the over-production of NO under the development of histamine-induced gastric damage in rats with partial vascular occlusion. Indeed, Tanaka et al (39) reported that NO significantly suppressed basal gastric acid secretion in an ischemiareperfusion model in pylorus-ligated rats. Yasuhiro et al (40) reported that L-NAME (10 -20 mg /kg, p.o.)…”

Section: Discussionmentioning

confidence: 99%

On the Mechanisms Underlying Histamine Induction of Gastric Mucosal Lesions in Rats With Partial Gastric Vascular Occlusion

Amagase

Okabe

2003

J Pharmacol Sci

View full text Add to dashboard Cite

Abstract. Although it is well known that histamine induces gastric mucosal lesions in laboratory animals, the fundamental mechanisms remain unclear. In order to further analyze the vascular mechanisms underlying histamine-induced lesions, a new model was developed in the glandular stomach via administration of histamine (40 mg / kg, s.c.) twice to rats with partial gastric vascular occlusion (ligated left gastric artery and vein) also subjected to pylorus ligation. Both antagonists of histamine H 2 -receptors (roxatidine and famotidine) and H 1 -receptors (epinastine and tripelennamine) significantly inhibited lesion formation at doses that did not inhibit acid secretion. Combined treatment of tripelennamine and famotidine synergistically inhibited lesion formation. Nitro L-arginine methyl ester inhibited lesion development; inhibition was reversed by concomitantly administered L-arginine. Indomethacin, diclofenac, and SC-560 (a selective COX-1 inhibitor), but not rofecoxib (a selective COX-2 inhibitor), significantly inhibited lesion formation. In addition, sodium bicarbonate, pirenzepine, S-0509 (a gastrin / CCK 2 inhibitor), omeprazole, sucralfate, and a prostaglandin analog also significantly inhibited lesion formation. It was concluded that the mechanism by which histamine induces gastric lesions in rats with partial gastric vascular occlusion appears to involve extensive vasodilation resulting from histamine acting on microvasculature histamine H 1 -and H 2 -receptors, generation of endogenous nitric oxide and prostaglandins, with the presence of gastric acid.

show abstract

The role of nitric oxide in the gastric acid secretion induced by ischemia–reperfusion in the pylorus-ligated rat

Cited by 27 publications

References 18 publications

Dual Action of Nitric Oxide in the Pathogenesis of Ischemia/Reperfusion-Induced Mucosal Injury in Mouse Stomach

Dual Action of Nitric Oxide in the Pathogenesis of Ischemia/Reperfusion-Induced Mucosal Injury in Mouse Stomach

Preventive and curative effects of curcumin on the development of gastric inflammatory diseases in rats

On the Mechanisms Underlying Histamine Induction of Gastric Mucosal Lesions in Rats With Partial Gastric Vascular Occlusion

Contact Info

Product

Resources

About