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Titolo:
A ROLE FOR CALCITONIN-GENE-RELATED PEPTIDE IN PROTECTION AGAINST GASTRIC-ULCERATION
Autore:
GRAY JL; BUNNETT NW; ORLOFF SL; MULVIHILL SJ; DEBAS HT;
Indirizzi:
UNIV CALIF SAN FRANCISCO,DEPT SURG U122,533 PARNASSUS AVE SAN FRANCISCO CA 94143 UNIV CALIF SAN FRANCISCO,DEPT SURG U122 SAN FRANCISCO CA 94143 UNIV CALIF SAN FRANCISCO,DEPT PHYSIOL SAN FRANCISCO CA 94143
Titolo Testata:
Annals of surgery
fascicolo: 1, volume: 219, anno: 1994,
pagine: 58 - 64
SICI:
0003-4932(1994)219:1<58:ARFCPI>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
INTRAGASTRIC CAPSAICIN PROTECTS; PERFUSED RAT STOMACH; ACID-SECRETION; SUBSTANCE-P; BLOOD-FLOW; RELEASE; STIMULATION; NEURONS; POTENT; DAMAGE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
24
Recensione:
Indirizzi per estratti:
Citazione:
J.L. Gray et al., "A ROLE FOR CALCITONIN-GENE-RELATED PEPTIDE IN PROTECTION AGAINST GASTRIC-ULCERATION", Annals of surgery, 219(1), 1994, pp. 58-64

Abstract

Objective The goal of this investigation was to determine the role ofcalcitonin gene-related peptide (CGRP) in gastric mucosal resistance to ulceration. Summary Background Data CGRP is a 37-amino acid peptidefound in the peripheral ends of afferent gastric neurons. CGRP is known to inhibit acid secretion, stimulate mucosal blood flow, and stimulate release of somatostatin. Methods The release of CGRP in response to intragastric and intra-arierial administration of capsaicin in the isolated, vascularly perfused rat stomach was measured by radioimmunoassay. The molecular forms of CGRP released were analyzed by gel filtration chromatography. The effect of intravenous CGRP or intragastric capsaicin on gastric ulceration induced by 100 mmol/L HCI and indomethacin was studied in intact and endogenous CGRP-depieted rats. Results Intra-arierial capsaicin (concentration range, 10(-7) to 10(-5) mol/L) stimulated a prompt and sustained release of immunoreactive CGRP, of which 84% coeluted with rat 1-37 CGRP I by gel filtration. Intragastric capsaicin (range, 10(-5) to 10(-4) mol/L) failed to release CGRP into the vascular perfusate. In intact rats, intragastric capsaicin (10(-6) mol/L) or intravenous CGRP I (10 mu g/kg/hr) reduced the number and area of mucosal lesions caused by HCI and indomethacin compared with thefindings in control rats. Rats depleted of endogenous CGRP were more susceptible to gastric ulceration than were normal rats. Intragastric capsaicin failed to protect the mucosa of CGRP-depleted rats, whereas exogenous intravenous CGRP was effective. Conclusions These data support the hypothesis that CGRP released from gastric enteric neurons mediates gastric mucosal resistance to ulceration by noxious agents.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 24/11/20 alle ore 11:12:57