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Titolo:
ROLE OF NITRIC-OXIDE IN MUCOSAL BLOOD-FLOW RESPONSE AND THE HEALING OF HCL-INDUCED LESIONS IN THE RAT STOMACH
Autore:
TAKEUCHI K; KATO S; TAKEHARA K; ASADA Y; YASUHIRO T;
Indirizzi:
KYOTO PHARMACEUT UNIV,DEPT PHARMACOL & EXPT THERAPEUT YAMASHINA KYOTO607 JAPAN
Titolo Testata:
Digestion
fascicolo: 1, volume: 58, anno: 1997,
pagine: 19 - 27
SICI:
0012-2823(1997)58:1<19:RONIMB>2.0.ZU;2-X
Fonte:
ISI
Lingua:
ENG
Soggetto:
GENE-RELATED PEPTIDE; ACID BACK-DIFFUSION; GASTRIC MICROCIRCULATION; SENSORY NEURONS; L-ARGININE; INJURY; CAPSAICIN; ULCERS; HYPEREMIA; SECRETION;
Keywords:
NITRIC OXIDE; GASTRIC LESION; HEALING; RAT; N-G-NITRO-L-ARGININE METHYL ESTER; GASTRIC MUCOSAL BLOOD FLOW;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
30
Recensione:
Indirizzi per estratti:
Citazione:
K. Takeuchi et al., "ROLE OF NITRIC-OXIDE IN MUCOSAL BLOOD-FLOW RESPONSE AND THE HEALING OF HCL-INDUCED LESIONS IN THE RAT STOMACH", Digestion, 58(1), 1997, pp. 19-27

Abstract

The role of nitric oxide (NO) in the gastric mucosal blood flow response and the healing of HCl-induced gastric lesions was investigated inrats. After 18 h fasting rats were given 0.6 N HCl p.o. for the induction of gastric lesions, and 1 h later they were fed normally. After induction of gastric lesions, they were repeatedly administered the NO synthase inhibitors N-G-nitro-L-arginine methyl ester (L-NAME 5-20 mg/kg p.o. twice daily) or aminoguanidine (20 mg/kg s.c. once daily) for 7 days. Gastric lesions caused by HCl healed almost completely within 5 days with granulation and to an extent with reepithelialization. Repeated administration of L-NAME but not aminoguanidine significantly delayed the healing of gastric lesions in a dose-dependent manner. The damaged mucosa secreted less acid, but showed a marked rise in H+ permeability, resulting in luminal acid loss accompanied by an increase of mucosal blood flow. Aminoguanidine did not significantly affect any ofthese functional changes observed in the stomach after damage by HCl,whereas L-NAME treatment slightly reversed the decreased acid response, increased the luminal H+ loss, and totally inhibited the mucosal hyperemic response associated with luminal acid loss in the damaged mucosa. In addition, the deleterious influences of L-NAME on the mucosal blood flow response and the healing of gastric lesions were significantly antagonized by co-administration of L-arginine but not of D-arginine (500 mg/kg x 2, i.p.). Luminal output of NO2-/NO3- was significantlyincreased in pylorus-ligated stomachs in control rats on days 3 and 5after damage, and such increases in gastric NO output were completelyattenuated by L-NAME treatment. These results suggest that endogenousNO may contribute to the healing of acute gastric injury by mediatingthe mucosal hyperemic responses associated with acid back-diffusion and by facilitating acid disposal in the damaged mucosa. NO mediating such responses and participating in the healing aspect of gastric lesions may be produced by the constitutive type of NO synthase.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/11/20 alle ore 12:49:07