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Titolo:
THE CHOLECYSTOKININ RECEPTOR ANTAGONIST L-364,718 REDUCES TAUROCHOLATE-INDUCED PANCREATITIS IN RATS
Autore:
KIM KH; LEE MG; KIM DG;
Indirizzi:
YONSEI UNIV,COLL MED,DEPT PHARMACOL SEOUL 120752 SOUTH KOREA
Titolo Testata:
International journal of pancreatology
fascicolo: 3, volume: 20, anno: 1996,
pagine: 205 - 211
SICI:
0169-4197(1996)20:3<205:TCRALR>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACUTE HEMORRHAGIC-PANCREATITIS; ENZYME-SECRETION; MICE; TRYPSIN; LOXIGLUMIDE; KALLIKREIN; CAMOSTATE; THROMBIN; PLASMIN;
Keywords:
ACUTE PANCREATITIS; L-364,718; CAMOSTAT; CHOLECYSTOKININ;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
35
Recensione:
Indirizzi per estratti:
Citazione:
K.H. Kim et al., "THE CHOLECYSTOKININ RECEPTOR ANTAGONIST L-364,718 REDUCES TAUROCHOLATE-INDUCED PANCREATITIS IN RATS", International journal of pancreatology, 20(3), 1996, pp. 205-211

Abstract

Conclusion. Our results suggest that the cholecystokinin (CCK) receptor antagonist L-364,718 has a protective effect on taurocholate-induced pancreatitis, and thus, it is inferred that CCK may have a significant pathophysiological role in the early phase of pancreatitis. Background. Conflicting results have been obtained from studies designed to determine the role of CCK in the initial stages of pancreatitis. Methods. We evaluated the protective effect of the CCK receptor antagonist L-364,718 (devazepide) and of the trypsin inhibitor camostat, on taurocholate-induced pancreatitis in rats. L-364,718 (1 mg/kg) or camostat (200 mg/kg) was administered intragastrically 30 min before the induction of pancreatitis. Results. Infusion of sodium taurocholate (50 mg/kg) into the pancreaticobiliary duct caused severe pancreatitis with marked hyperamylasemia and reduction of tissue enzyme content at 12 h postinfusion. Pretreatment with L-364,718, but not with camostat, caused significant improvement in signs of experimental pancreatitis based ontissue enzyme content and morphology. Compared with untreated pancreatitis, there was relatively well-preserved lobular architecture, less edema, less infiltration of inflammatory cells, and more zymogen granules after L-364,718 pretreatment. Moreover, the reduction of enzyme content owing to pancreatitis was ameliorated by L-364,718 pretreatment.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/11/20 alle ore 16:54:19