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Titolo:
DEVAZEPIDE-INDUCED HYPERPLASIA IN THE RAT-LIVER AND BILE-DUCTS
Autore:
OHLSSON B; AXELSON J; REHFELD JF; IHSE I;
Indirizzi:
UNIV LUND HOSP,DEPT SURG S-22185 LUND SWEDEN UNIV LUND HOSP,DEPT SURG S-22185 LUND SWEDEN RIGSHOSP,DEPT CLIN BIOCHEM DK-2100 COPENHAGEN DENMARK
Titolo Testata:
European surgical research
fascicolo: 4, volume: 28, anno: 1996,
pagine: 299 - 305
SICI:
0014-312X(1996)28:4<299:DHITRA>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
FOOD-INTAKE; CHOLECYSTOKININ ANTAGONIST; REGENERATION; INHIBITION; PROGLUMIDE; MECHANISM; DIVERSION; SECRETION; PEPTIDES; POTENT;
Keywords:
BILE DUCTS; CHOLECYSTOKININ; DEVAZEPIDE; LIVER; TROPHIC EFFECTS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
31
Recensione:
Indirizzi per estratti:
Citazione:
B. Ohlsson et al., "DEVAZEPIDE-INDUCED HYPERPLASIA IN THE RAT-LIVER AND BILE-DUCTS", European surgical research, 28(4), 1996, pp. 299-305

Abstract

Cholecystokinin (CCK) is a potent stimulus of pancreatic enzyme secretion and growth and is known to influence the flow of biliary secretions. It has also been suggested as a trophic stimulus of the biliary tract and liver, but confirmatory studies are lacking. The aim of the present experiment was to study the effects on the rat liver and biliarytract of long-term stimulation of CCK-8S and the CCK-A receptor antagonist devazepide, respectively. Sprague-Dawley male rats had an infusion of sulfated CCK-8, devazepide or sodium chloride by subcutaneously implanted osmotic minipumps. The animals were sacrified 36 h and 3, 7 or 28 days after the start of infusion, and all had an injection of tritiated thymidine (1 mCi/kg) intraperitoneally 1 h prior to death. Theliver was dissected out, weighed and processed for its content of protein, DNA and water. After autoradiography, histologic samples were examined for labeled hepatocytes and bile duct epithelium. Devazepide caused an increase in liver protein content from 36 h on. After 3 days labeling index of hepatocytes and liver DNA concentration were increased. On day 7, induced cell proliferation was also seen in the bile ductepithelium, and the increase in liver DNA content and concentration was now more pronounced and persisted throughout the study. After 28 days devazepide also induced increased crude and relative liver weight. A transient reduction in liver weight and liver protein content and concentration was seen after 7 days of CCK-8S infusion. There were no changes of the labeling index of hepatocytes or bile duct epithelial cells or in liver DNA content in the rats receiving CCK-8S infusion. Devazepide induced hyperplastic changes in both the liver and the biliary tract, probably by interfering with the bile secretion, whereas CCK-8Sdid not exert any similar effects. The results do not support CCK as a hepatotrophic factor.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 23/09/20 alle ore 12:50:51